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The utilization of 3D cell culture for spheroid formation holds significant implications in cancer research, contributing to a fundamental understanding of the disease and aiding drug development. Conventional methods such as the hanging drop technique and other alternatives encounter limitations due to smaller drop volumes, leading to nutrient starvation and restricted culture duration. In this study, we present a straightforward approach to creating superhydrophobic paper cones capable of accommodating large volumes of culture media drops. These paper cones have sterility, autoclavability, and bacterial repellent properties. Leveraging these attributes, we successfully generate large spheroids of ovarian cancer cells and, as a proof of concept, conduct drug screening to assess the impact of carboplatin. Thus, our method enables the preparation of flexible superhydrophobic surfaces for laboratory applications in an expeditious manner, exemplified here through spheroid formation and drug screening demonstrations. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) are important cell-to-cell communication mediators. This paper focuses on the regulatory role of tumor-derived EVs on macrophages. It aims to investigate the causes of tumor progression and therapeutic directions. Tumor-derived EVs can cause macrophages to shift to M1 or M2 phenotypes. This indicates they can alter the M1/M2 cell ratio and have pro-tumor and antiinflammatory effects. This paper discusses several key points: first, the factors that stimulate macrophage polarization and the cytokines released as a result; second, an overview of EVs and the methods used to isolate them; third, how EVs from various cancer cell sources, such as hepatocellular carcinoma, colorectal carcinoma, lung carcinoma, breast carcinoma, and glioblastoma cell sources carcinoma, promote tumor development by inducing M2 polarization in macrophages; and fourth, how EVs from breast carcinoma, pancreatic carcinoma, lungs carcinoma, and glioblastoma cell sources carcinoma also contribute to tumor development by promoting M2 polarization in macrophages. Modified or sourced EVs from breast, pancreatic, and colorectal cancer can repolarize M2 to M1 macrophages. This exhibits anti-tumor activities and offers novel approaches for tumor treatment. Therefore, we discovered that macrophage polarization to either M1 or M2 phenotypes can regulate tumor development. This is based on the description of altering macrophage phenotypes by vesicle contents. [ABSTRACT FROM AUTHOR]

Understand the dynamics of cancer stem cells (CSCs), prevent the non-recurrence of cancers and develop therapeutic strategies to destroy both cancer cells and CSCs remain a challenge topic. In this paper, we study both analytically and numerically the dynamics of CSCs under radiotherapy effects. The dynamical model takes into account the diffusion of cells, the de-differentiation (or plasticity) mechanism of differentiated cancer cells (DCs) and the time delay on the interaction between microRNAs molecules (microRNAs) with DCs. The stability of the model system is studied by using a Hopf bifurcation analysis. We mainly investigate on the critical time delay τ c , that represents the time for DCs to transform into CSCs after the interaction of microRNAs with DCs. Using the system parameters, we calculate the value of τ c for prostate, lung and breast cancers. To confirm the analytical predictions, the numerical simulations are performed and show the formation of spatiotemporal circular patterns. Such patterns have been found as promising diagnostic and therapeutic value in management of cancer and various diseases. The radiotherapy is applied in the particular case of prostate model. We calculate the optimum dose of radiation and determine the probability of avoiding local cancer recurrence after radiotherapy treatment. We find numerically a complete eradication of patterns when the radiotherapy is applied before a time t < τ c . This scenario induces microRNAs to act as suppressors as experimentally observed in prostate cancer. The results obtained in this paper will provide a better concept for the clinicians and oncologists to understand the complex dynamics of CSCs and to design more efficacious therapeutic strategies to prevent the non-recurrence of cancers. [ABSTRACT FROM AUTHOR]

As a promising cancer treatment method, cold atmospheric plasma has received widespread attention in recent years. However, previous research has focused more on how to realize and expand the anti-cancer scope of plasma jet. There are also studies on the killing of small-scale cancer cells, but the effects of plasma jet on normal cells and normal cell clusters have been ignored. Therefore, we proposed a 50 µm sized micro-plasma jet device, and used the device to treat melanoma cells (A-375) and human glial cells (HA1800) to evaluate their anti-cancer effects and effects on normal cells. The experimental results show that this kind of micro-plasma jet device can effectively inactivate cancer cells in a short period of time, while having little effect on normal cells. This work provides a certain experimental basis for the application of fine plasma jet to clinically inactivate cancer cells. ARTICLE HIGHLIGHTS: HIGHLIGHTS • The experiment of apoptosis induced by plasma jet was carried out in this paper. A-375 and HA1800 were treated with plasma jet and subsequently characterized. • Based on the experimental results of this paper, it can be concluded that plasma jet has a significant role in inducing apoptosis. • The ability of plasma jet to induce apoptosis of cancer cells is much higher than that of normal cells. [ABSTRACT FROM AUTHOR]

Primary tumors can inhibit the growth of secondary lesions, particularly metastases, in a phenomenon termed "concomitant resistance". Several mechanisms have been proposed for this effect, each supported by experimental data. In this paper, we hypothesize that concomitant resistance is a form of hormesis, a biphasic dose response in which a stimulus has a positive and/or stimulatory effect at low dosages and a negative, inhibitory, and/or toxic effect at higher dosages. When this paradigm applies to tumorigenesis, it is referred to as "cancer hormesis". Thus, low numbers of benign neoplastic cells or less tumorigenic malignant cells may result in resistance to the development of malignant neoplasms, including metastases. A host containing a number of (less tumorigenic) neoplastic cells may exhibit greater protection against more tumorigenic malignant neoplasms than a host who lacks neoplastic cells, or who has too few neoplastic cells to stimulate a protective response. As a theoretical endeavor, this paper also proposes that cancer hormesis can be leveraged for therapeutic purposes, by the implantation of safely controlled, benign artificial tumors in high-risk patients. These tumors would prevent the development of endogenous malignant neoplasms by creating an inhibitory environment for such growth. Strategies for testing the hypothesis are proposed. [ABSTRACT FROM AUTHOR]

The article titled "[Retracted] Anthelmintic drug albendazole arrests human gastric cancer cells at the mitotic phase and induces apoptosis" has been retracted from the journal Experimental & Therapeutic Medicine. A concerned reader brought to the editor's attention that there were similarities in the data presented in the flow cytometric experiments that were difficult to attribute to coincidence. After an internal investigation, the editor verified the claims and decided to retract the paper due to a lack of confidence in the presented data. The authors were contacted and accepted the decision to retract the paper, except for one author who could not be reached. The editor apologizes for any inconvenience caused. [Extracted from the article]

This article, published in Oncology Letters, discusses the role of ATP-binding cassette transporter A7 (ABCA7) in promoting epithelial-to-mesenchymal transition (EMT) in ovarian cancer cells by upregulating the transforming growth factor-β (TGF-β) signaling pathway. However, the paper has been retracted due to concerns raised by a reader regarding the similarity of certain data in Figure 4C to data published in another article by different authors. The authors were asked for an explanation but did not respond. The Editor has decided to retract the paper and apologizes for any inconvenience caused. [Extracted from the article]

This article, titled "[Retracted] Nicotinamide N‑methyltransferase promotes epithelial‑mesenchymal transition in gastric cancer cells by activating transforming growth factor‑β1 expression," was published in Oncology Letters in 2018. However, it has since been retracted due to concerns raised by a reader. The reader pointed out that the western blotting data, scratch-wound assay data, and migration and invasion assay data presented in the article were similar to data from previously published articles by different authors or articles submitted for publication around the same time. Additionally, two data panels in the cell morphological images were found to be overlapping. The authors accepted the decision to retract the paper, and the editor apologizes for any inconvenience caused. [Extracted from the article]

Combination therapy is well established as a key intervention strategy for cancer treatment, with the potential to overcome monotherapy resistance and deliver a more durable efficacy. However, given the scale of unexplored potential target space and the resulting combinatorial explosion, identifying efficacious drug combinations is a critical unmet need that is still evolving. In this paper, we demonstrate a network biology-driven, simulation-based solution, the Simulated Cell™. Integration of omics data with a curated signaling network enables the accurate and interpretable prediction of 66,348 combination-cell line pairs obtained from a large-scale combinatorial drug sensitivity screen of 684 combinations across 97 cancer cell lines (BAC = 0.62, AUC = 0.7). We highlight drug combination pairs that interact with DNA Damage Response pathways and are predicted to be synergistic, and deep network insight to identify biomarkers driving combination synergy. We demonstrate that the cancer cell 'avatars' capture the biological complexity of their in vitro counterparts, enabling the identification of pathway-level mechanisms of combination benefit to guide clinical translatability. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) are recruited by malignant tumor cells to the tumor microenvironment (TME) and play a crucial role in the initiation and progression of malignant tumors. This role encompasses immune evasion, promotion of angiogenesis, stimulation of cancer cell proliferation, correlation with cancer stem cells, multilineage differentiation within the TME, and development of treatment resistance. Simultaneously, extensive research is exploring the homing effect of MSCs and MSC‐derived extracellular vesicles (MSCs‐EVs) in tumors, aiming to design them as carriers for antitumor substances. These substances are targeted to deliver antitumor drugs to enhance drug efficacy while reducing drug toxicity. This paper provides a review of the supportive role of MSCs in tumor progression and the associated molecular mechanisms. Additionally, we summarize the latest therapeutic strategies involving engineered MSCs and MSCs‐EVs in cancer treatment, including their utilization as carriers for gene therapeutic agents, chemotherapeutics, and oncolytic viruses. We also discuss the distribution and clearance of MSCs and MSCs‐EVs upon entry into the body to elucidate the potential of targeted therapies based on MSCs and MSCs‐EVs in cancer treatment, along with the challenges they face. [ABSTRACT FROM AUTHOR]

Lorlatinib is a pharmaceutical ALK kinase inhibitor used to treat ALK driven non-small cell lung cancers. This paper analyses the intersection of past published data on the physiological consequences of two unrelated drugs from general medical practice—itraconazole and cilostazol—with the pathophysiology of ALK positive non-small cell lung cancer. A conclusion from that data analysis is that adding itraconazole and cilostazol may make lorlatinib more effective. Itraconazole, although marketed worldwide as a generic antifungal drug, also inhibits Hedgehog signaling, Wnt signaling, hepatic CYP3A4, and the p-gp efflux pump. Cilostazol, marketed worldwide as a generic thrombosis preventative drug, acts by inhibiting phosphodiesterase 3, and, by so doing, lowers platelets' adhesion, thereby partially depriving malignant cells of the many tumor trophic growth factors supplied by platelets. Itraconazole may enhance lorlatinib effectiveness by (i) reducing or stopping a Hedgehog-ALK amplifying feedback loop, by (ii) increasing lorlatinib's brain levels by p-gp inhibition, and by (iii) inhibiting growth drive from Wnt signaling. Cilostazol, surprisingly, carries minimal bleeding risk, lower than that of aspirin. Risk/benefit assessment of the combination of metastatic ALK positive lung cancer being a low-survival disease with the predicted safety of itraconazole-cilostazol augmentation of lorlatinib favors a trial of this drug trio in ALK positive lung cancer. [ABSTRACT FROM AUTHOR]

(1) Background: The neddylation pathway assumes a pivotal role in the initiation and progression of cancer. MLN4924, a potent small-molecule inhibitor of the NEDD8-activating enzyme (NAE), effectively intervenes in the early stages of the neddylation pathway. By instigating diverse cellular responses, such as senescence and apoptosis in cancer cells, MLN4924 also exerts regulatory effects on non-malignant cells within the tumor microenvironment (TME) and tumor virus-infected cells, thereby impeding the onset of tumors. Consequently, MLN4924 has been widely acknowledged as a potent anti-cancer drug. (2) Recent findings: Nevertheless, recent findings have illuminated additional facets of the neddylation pathway, revealing its active involvement in various biological processes detrimental to the survival of cancer cells. This newfound understanding underscores the dual role of MLN4924 in tumor therapy, characterized by both anti-cancer and pro-cancer effects. This dichotomy is herein referred to as the "double-edged effects" of MLN4924. This paper delves into the intricate relationship between the neddylation pathway and cancer, offering a mechanistic exploration and analysis of the causes underlying the double-edged effects of MLN4924—specifically, the accumulation of pro-cancer neddylation substrates. (3) Perspectives: Here, the objective is to furnish theoretical support and novel insights that can guide the development of next-generation anti-cancer drugs targeting the neddylation pathway. [ABSTRACT FROM AUTHOR]

A novel cholic acid-conjugated carboplatin (CP-CA) is developed as a liver-targeting prodrug of carboplatin (CP) for liver cancer. Instead of using CP as a raw material, CP-CA was synthesized simultaneously. This paper is focused on the comparison of CP-CA and CP with respect to their pharmacokinetic (PK) and tissue distribution profiles in rats after their intravenous administration. Additionally, their uptake by human liver tumor cell Huh7 and normal human liver cell HL7702 are investigated. The inductively coupled plasma mass spectrometry (ICP-MS) method is applied for the determination of platinum in plasma, tissues, and cells. The PK results show that both the AUC0–t and AUC0–∞ data on Pt for CP-CA are significantly higher than those for CP (p < 0.01), indicating that the plasma exposure of CP-CA is significantly higher than that of CP. The CL1, Vd1, and Vd2 data on Pt for CP-CA are significantly lower than those for CP (p < 0.01), while the MRT0–t is significantly higher (p < 0.01), which is possibly related to a higher PPBR, and can strongly support the higher AUC0–t and AUC0–∞ of Pt for CP-CA compared to for CP. The tissue distribution results show that CP-CA is mainly distributed and accumulated in the liver after its intravenous administration to rats, revealing its liver-targeting profile. Compared to CP, CP-CA is more easily taken up by human liver cancer cells and normal human liver cells. The results suggest that CP-CA has a potential for further development as a new prodrug specific to liver cancer. [ABSTRACT FROM AUTHOR]

Natural killer (NK) cells, as innate lymphocytes, possess cytotoxic capabilities and engage target cells through a repertoire of activating and inhibitory receptors. Particularly, natural killer group 2, member D (NKG2D) receptor on NK cells recognizes stress‐induced ligands—the MHC class I chain‐related molecules A and B (MICA/B) presented on tumor cells and is key to trigger the cytolytic response of NK cells. However, tumors have developed sophisticated strategies to evade NK cell surveillance, which lead to failure of tumor immunotherapy. In this paper, we summarized these immune escaping strategies, including the downregulation of ligands for activating receptors, upregulation of ligands for inhibitory receptors, secretion of immunosuppressive compounds, and the development of apoptosis resistance. Then, we focus on recent advancements in NK cell immune therapies, which include engaging activating NK cell receptors, upregulating NKG2D ligand MICA/B expression, blocking inhibitory NK cell receptors, adoptive NK cell therapy, chimeric antigen receptor (CAR)‐engineered NK cells (CAR‐NK), and NKG2D CAR‐T cells, especially several vaccines targeting MICA/B. This review will inspire the research in NK cell biology in tumor and provide significant hope for improving cancer treatment outcomes by harnessing the potent cytotoxic activity of NK cells. [ABSTRACT FROM AUTHOR]

The article titled "Retraction: Regulation of circGOLPH3 and its binding protein CBX7 on the proliferation and apoptosis of prostate cancer cells" has been retracted from Bioscience Reports due to concerns raised about the figures in the paper. The Editorial Board received a notification from a reader pointing out that Figure 2B in the paper appeared as Figure 1C in a previous publication. Additionally, there were similarities between certain regions of different figures in the paper. The authors were contacted but did not respond, leading to the decision to retract the article. [Extracted from the article]

Background: Breast cancer (BC) is a heterogeneous neoplasm characterized by several subtypes. One of the most aggressive with high metastasis rates presents overexpression of the human epidermal growth factor receptor 2 (HER2). A quantitative evaluation of HER2 levels is essential for a correct diagnosis, selection of the most appropriate therapeutic strategy and monitoring the response to therapy. Results: In this paper, we propose the synergistic use of SERS and Raman technologies for the identification of HER2 expressing cells and its accurate assessment. To this end, we selected SKBR3 and MDA-MB-468 breast cancer cell lines, which have the highest and lowest HER2 expression, respectively, and MCF10A, a non-tumorigenic cell line from normal breast epithelium for comparison. The combined approach provides a quantitative estimate of HER2 expression and visualization of its distribution on the membrane at single cell level, clearly identifying cancer cells. Moreover, it provides a more comprehensive picture of the investigated cells disclosing a metabolic signature represented by an elevated content of proteins and aromatic amino acids. We further support these data by silencing the HER2 gene in SKBR3 cells, using the RNA interference technology, generating stable clones further analysed with the same combined methodology. Significant changes in HER2 expression are detected at single cell level before and after HER2 silencing and the HER2 status correlates with variations of fatty acids and downstream signalling molecule contents in the context of the general metabolic rewiring occurring in cancer cells. Specifically, HER2 silencing does reduce the growth ability but not the lipid metabolism that, instead, increases, suggesting that higher fatty acids biosynthesis and metabolism can occur independently of the proliferating potential tied to HER2 overexpression. Conclusions: Our results clearly demonstrate the efficacy of the combined SERS and Raman approach to definitely pose a correct diagnosis, further supported by the data obtained by the HER2 gene silencing. Furthermore, they pave the way to a new approach to monitor the efficacy of pharmacologic treatments with the aim to tailor personalized therapies and optimize patients' outcome. [ABSTRACT FROM AUTHOR]

Microfluidic devices have long been useful for both the modeling and diagnostics of numerous diseases. In the past 20 years, they have been increasingly adopted for helping to study those in the family of breast cancer through characterizing breast cancer cells and advancing treatment research in portable and replicable formats. This paper adds to the body of work concerning cancer-focused microfluidics by proposing a simulation of a hypothetical bi-ended three-pronged device with a single channel and 16 electrodes with 8 pairs under different voltage and frequency regimes using COMSOL. Further, a study was conducted to examine the frequencies most effective for ACEO to separate cancer cells and accompanying particles. The study revealed that the frequency of EF has a more significant impact on the separation of particles than the inlet velocity. Inlet velocity variations while holding the frequency of EF constant resulted in a consistent trend showing a direct proportionality between inlet velocity and net velocity. These findings suggest that optimizing the frequency of EF could lead to more effective particle separation and targeted therapeutic interventions for breast cancer. This study hopefully will help to create targeted therapeutic interventions by bridging the disparity between in vitro and in vivo models. [ABSTRACT FROM AUTHOR]

Natural killer cells (NKCs) are non-specific immune lymphocytes with diverse morphologies. Their broad killing effect on cancer cells has led to increased attention towards activating NKCs for anticancer immunotherapy. Consequently, understanding the motion characteristics of NKCs under different morphologies and modeling their collective dynamics under cancer cells has become crucial. However, tracking small NKCs in complex backgrounds poses significant challenges, and conventional industrial tracking algorithms often perform poorly on NKC tracking datasets. There remains a scarcity of research on NKC dynamics. In this paper, we utilize deep learning techniques to analyze the morphology of NKCs and their key points. After analyzing the shortcomings of common industrial multi-object tracking algorithms like DeepSORT in tracking natural killer cells, we propose Distance Cascade Matching and the Re-Search method to improve upon existing algorithms, yielding promising results. Through processing and tracking over 5000 frames of images, encompassing approximately 300,000 cells, we preliminarily explore the impact of NKCs' cell morphology, temperature, and cancer cell environment on NKCs' motion, along with conducting basic modeling. The main conclusions of this study are as follows: polarized cells are more likely to move along their polarization direction and exhibit stronger activity, and the maintenance of polarization makes them more likely to approach cancer cells; under equilibrium, NK cells display a Boltzmann distribution on the cancer cell surface. [ABSTRACT FROM AUTHOR]

Cancer diseases constitute a major health problem which leads to the death of millions of people annually. They are unique among other diseases because cancer cells can perfectly adapt to the environment that they create themselves. This environment is usually highly hostile and for normal cells it would be hugely difficult to survive, however neoplastic cells not only can survive but also manage to proliferate. One of the reasons is that they can alter immunological pathways which allow them to be flexible and change their phenotype to the one needed in specific conditions. The aim of this paper is to describe some of these immunological pathways that play significant roles in gynecologic neoplasms as well as review recent research in this field. It is of high importance to possess extensive knowledge about these processes, as greater understanding leads to creating more specialized therapies which may prove highly effective in the future. [ABSTRACT FROM AUTHOR]

Tumor dormancy is a stage in the growth and development of malignant cells and is one of the biological characteristics of malignant cells. Complex transitions involving dormant tumor cells between quiescent and proliferative states pose challenges for tumor eradication. This paper explores the biological features and molecular mechanisms of tumor dormancy and highlights emerging therapies. The strategies discussed promise innovative clinical potential against malignant tumors. Understanding the mechanisms of dormancy can help provide valuable insights into the diagnosis and treatment of malignant tumors to advance the fight against this world problem. [ABSTRACT FROM AUTHOR]

Simple Summary: A large body of multidisciplinary evidence involves the topic of thyroid cancer (the most common endocrine malignancy). Nevertheless, exceptional findings such as thyroid cancer in ectopic thyroid tissue, representing 0.3–0.5% of the malignant neoplasia with any location, suggest even greater challenges. Awareness remains the key operative element since the index of suspicion is low, especially in non-cervical areas. Hence, currently, the ectopic thyroid remains a matter of individualized management. The ectopic mediastinal thyroid (EMT) is part of the less frequent sublingual ectopic sites. Here, we introduce the most complex analysis in published EMT data (N = 117 patients) that identified an unexpectedly high rate of malignancy (18.8%), papillary cancer being the most frequent histological type. A rate of 5.98% amid all EMTs represented individuals confirmed with unrelated (non-thyroid) malignancies. Thyroid anomalies (other than EMT presence) were reported in 38.33% of the benign EMT, while the overall malignancy rate in EMTs was higher than expected according to prior data when compared to other ectopic sites. We aimed to analyze the management of the ectopic mediastinal thyroid (EMT) with respect to EMT-related cancer and non-malignant findings related to the pathological report, clinical presentation, imaging traits, endocrine profile, connective tissue to the cervical (eutopic) thyroid gland, biopsy or fine needle aspiration (FNA) results, surgical techniques and post-operatory outcome. This was a comprehensive review based on revising any type of freely PubMed-accessible English, full-length original papers including the keywords "ectopic thyroid" and "mediastinum" from inception until March 2024. We included 89 original articles that specified EMTs data. We classified them into four main groups: (I) studies/case series (n = 10; N = 36 EMT patients); (II) malignant EMTs (N = 22 subjects; except for one newborn with immature teratoma in the EMT, only adults were reported; mean age of 62.94 years; ranges: 34 to 90 years; female to male ratio of 0.9). Histological analysis in adults showed the following: papillary (N = 11/21); follicular variant of the papillary type (N = 2/21); Hürthle cell thyroid follicular malignancy (N = 1/21); poorly differentiated (N = 1/21); anaplastic (N = 2/21); medullary (N = 1/21); lymphoma (N = 2/21); and MALT (mucosa-associated lymphoid tissue) (N = 1/21); (III) benign EMTs with no thyroid anomalies (N = 37 subjects; mean age of 56.32 years; ranges: 30 to 80 years; female to male ratio of 1.8); (IV) benign EMTs with thyroid anomalies (N = 23; female to male ratio of 5.6; average age of 52.1 years). This panel involved clinical/subclinical hypothyroidism (iatrogenic, congenital, thyroiditis-induced, and transitory type upon EMT removal); thyrotoxicosis (including autonomous activity in EMTs that suppressed eutopic gland); autoimmune thyroiditis/Graves's disease; nodules/multinodular goiter and cancer in eutopic thyroid or prior thyroidectomy (before EMT detection). We propose a 10-item algorithm that might help navigate through the EMT domain. To conclude, across this focused-sample analysis (to our knowledge, the largest of its kind) of EMTs, the EMT clinical index of suspicion remains low; a higher rate of cancer is reported than prior data (18.8%), incident imagery-based detection was found in 10–14% of the EMTs; surgery offered an overall good outcome. A wide range of imagery, biopsy/FNA and surgical procedures is part of an otherwise complex personalized management. [ABSTRACT FROM AUTHOR]

Background: Ubiquitin-conjugating enzyme E2 N (UBE2N) is recognized in the progression of some cancers; however, little research has been conducted to describe its role in prostate cancer. The purpose of this paper is to explore the function and mechanism of UBE2N in prostate cancer cells. Methods: UBE2N expression was detected in Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD) data, prostate cancer tissue microarrays, and prostate cancer cell lines, respectively. UBE2N knockdown or overexpression was used to analyze its role in cell viability and glycolysis of prostate cancer cells and tumor growth. XAV939 or Axin1 overexpression was co-treated with UBE2N overexpression to detect the involvement of the Wnt/β-catenin signaling and Axin1 in the UBE2N function. UBE2N interacting with Axin1 was analyzed by co-immunoprecipitation assay. Results: UBE2N was upregulated in prostate cancer and the UBE2N-high expression correlated with the poor prognosis of prostate cancer. UBE2N knockdown inhibited cell viability and glycolysis in prostate cancer cells and restricted tumor formation in tumor-bearing mice. Wnt/β-catenin inhibition and Axin1 overexpression reversed the promoting viability and glycolysis function of UBE2N. UBE2N promoted Axin1 ubiquitination and decreased Axin1 protein level. Significance: Abnormally high expression of UBE2N acts as a cancer promoter to strengthen glycolysis and viability of prostate cancer cells. The mechanism of UBE2N is its promotion of the ubiquitination of Axin1. [ABSTRACT FROM AUTHOR]

Background: Cancer cells in lymph nodes can undergo metabolic changes, producing acidic byproducts. Our previous experimental results demonstrated significant pH differences between involved and free lymph nodes (LNs), potentially attributed to the release of these acidic byproducts. However, the accuracy of frozen sections is influenced by pathologists' expertise and limited response time. To address these limitations, we developed a simple pH sensing method. Methods: We conduct a cross-sectional study on non-neoadjuvant breast cancer patients (n= 34) from Shohada Tjarish Hospital and Azar Surgical Clinic to check the agreement between the pH value of sentinel lymph nodes (SLNs) and their pathologic score. To assess the pH assay's validity in detecting metastasized cancer cells in lymph nodes, the sensitivity, specificity, and accuracy of the sensor were calculated using Permanent pathology of LNs as the reference standard. Results: The results showed that cancer SLNs had pH≤ 7, while free LNs had pH > 8 (P-value <0.001). The sensitivity and specificity of the data were 89% (95% CI (0.73-1.05)) and 82% (95% CI (0.64-1.00)), respectively. Conclusion: Hence, in the absence of a frozen section, such a simple measurement may assist the surgeon in deciding whether to dissect more LNs or not. [ABSTRACT FROM AUTHOR]

Plant viral nanoparticles (VNPs) are attractive to nanomedicine researchers because of their safety, ease of production, resistance, and straightforward functionalization. In this paper, we developed and successfully purified a VNP derived from turnip mosaic virus (TuMV), a well-known plant pathogen, that exhibits a high affinity for immunoglobulins G (IgG) thanks to its functionalization with the Z domain of staphylococcal Protein A via gene fusion. We selected cetuximab as a model IgG to demonstrate the versatility of this novel TuMV VNP by developing a fluorescent nanoplatform to mark tumoral cells from the Cal33 line of a tongue squamous cell carcinoma. Using confocal microscopy, we observed that fluorescent VNP–cetuximab bound selectively to Cal33 and was internalized, revealing the potential of this nanotool in cancer research. [ABSTRACT FROM AUTHOR]

Oral cancer is a common malignancy with a high mortality rate. Although surgery is the best treatment option for patients with cancer, this approach is ineffective for advanced metastases. Molecular agents are irreplaceable in preventing and treating distant metastases. This review aims to summarise the molecular agents used for the treatment of oral cancer in the last decade and describe their sources and curative effects. These agents are classified into phenols, isothiocyanates, anthraquinones, statins, flavonoids, terpenoids, and steroids. The mechanisms of action of these agents include regulating the expression of cell signalling pathways and related proteases to affect the proliferation, autophagy, migration, apoptosis, and other biological aspects of oral cancer cells. This paper may serve as a reference for subsequent studies on the treatment of oral cancer. [ABSTRACT FROM AUTHOR]

Objective: The aim of this paper is to investigate the effect of long noncoding RNA (lncRNA) MIR100HG on the proliferation and metastasis of lung cancer cells by mediating the microRNA (miR)−5590‐3p/DCBLD2 axis. Methods: RNA levels of MIR100HG, miR‐5590‐3p, and DCBLD2 in lung cancer tissues and cells were detected by quantitative reverse‐transcription polymerase chain reaction, and protein level was assessed by Western blot. Effects of MIR100HG or miR‐5590‐3p on proliferation, migration, and invasion of lung cancer cells were detected by Cell Counting Kit‐8, colony formation, and Transwell assays. Luciferase reporter assay and RNA‐immunoprecipitation assay confirmed the target relationship between miR‐5590‐3p and MIR100HG or DCBLD2. Results: MIR100HG and DCBLD2 were highly expressed, while miR‐5590‐3p was lowly expressed in lung cancer tissues and cells. Silencing MIR100HG or upregulating miR‐5590‐3p impeded lung cancer cell proliferation, migration, and invasion. MIR100HG could up‐regulate DCBLD2 by sponging miR‐5590‐3p. Downregulation of miR‐5590‐3p partly overturned the suppressive effect of silencing MIR100HG on lung cancer cell proliferation and metastasis, and overexpression of DCBLD2 also reversed the effect of overexpression of miR‐5590‐3p on lung cancer cell proliferation and metastasis. Conclusion: LncRNA MIR100HG promotes lung cancer progression by targeting and negatively regulating DCBLD2 through binding with miR‐5590‐3p. [ABSTRACT FROM AUTHOR]

This article, titled "[Retracted] miR-124 inhibits proliferation, migration and invasion of malignant melanoma cells via targeting versican," was published in the journal Experimental & Therapeutic Medicine in 2017. However, it has since been retracted due to concerns raised by a reader. The reader pointed out that certain data in the article appeared to be similar to data from other articles written by different authors at different research institutes. The editor of the journal decided to retract the paper, and despite being asked for an explanation, the authors did not respond. The editor apologizes for any inconvenience caused. [Extracted from the article]

This article, titled "[Retracted] MicroRNA-203 inhibits malignant melanoma cell migration by targeting versican," was published in the journal Experimental & Therapeutic Medicine in 2014. However, it has since been retracted due to concerns raised by a reader. The reader pointed out that the western blotting data and Transwell migration assay data presented in the article were similar to data from other articles written by different authors at different research institutes. The editor of the journal decided to retract the paper, and the authors did not provide an explanation for these concerns. The editor apologizes for any inconvenience caused. [Extracted from the article]

Fluorine-18 fluorodeoxyglucose ([18F]FDG) is nowadays the leading positron emission tomography (PET) tracer for routine clinical work-ups in hematological malignancies; however, it is limited by false positive findings. Notably, false positives can occur in inflammatory and infective cases or in necrotic tumors that are infiltrated by macrophages and other inflammatory cells. In this context, 3′-deoxy-3′-[18F]fluorothymidine ([18F]FLT) has been shown to be a promising imaging biomarker of hematological malignant cell proliferation. In this review, a total of 15 papers were reviewed to collect literature data regarding the clinical application of [18F]FLT PET/CT in hematological malignancies. This imaging modality seems to be a suitable tool for noninvasive assessment of tumor grading, also showing a correlation with Ki-67 immunostaining. Moreover, [18F]FLT PET/CT demonstrated high sensitivity in detecting aggressive lymphoma lesions, especially when applying a standardized uptake value (SUV) cutoff of 3. At baseline, the potential of [18F]FLT imaging as a predictive tool is demonstrated by the low tracer uptake in patients with a complete response. However, its use is limited in evaluating bone diseases due to its high physiological uptake in bone marrow. Interim [18F]FLT PET/CT (iFLT) has the potential to identify high-risk patients with greater precision than [18F]FDG PET/CT, optimizing risk-adapted therapy strategies. Moreover, [18F]FLT uptake showed a greater ability to differentiate tumor from inflammation compared to [18F]FDG, allowing the reduction of false-positive findings and making the first one a more selective tracer. Finally, FLT emerges as a superior independent predictor of PFS and OS compared to FDG and ensures a reliable early response assessment with greater accuracy and predictive value. [ABSTRACT FROM AUTHOR]

Myeloid-derived suppressor cells (MDSCs) are key immunosuppressive cells in the tumor microenvironment (TME) that play critical roles in promoting tumor growth and metastasis. Tumor-associated platelets (TAPs) help cancer cells evade the immune system and promote metastasis. In this paper, we describe the interaction between MDSCs and TAPs, including their generation, secretion, activation, and recruitment, as well as the effects of MDSCs and platelets on the generation and changes in the immune, metabolic, and angiogenic breast cancer (BC) microenvironments. In addition, we summarize preclinical and clinical studies, traditional Chinese medicine (TCM) therapeutic approaches, and new technologies related to targeting and preventing MDSCs from interacting with TAPs to modulate the BC TME, discuss the potential mechanisms, and provide perspectives for future development. The therapeutic strategies discussed in this review may have implications in promoting the normalization of the BC TME, reducing primary tumor growth and distant lung metastasis, and improving the efficiency of anti-tumor therapy, thereby improving the overall survival (OS) and progression-free survival (PFS) of patients. However, despite the significant advances in understanding these mechanisms and therapeutic strategies, the complexity and heterogeneity of MDSCs and side effects of antiplatelet agents remain challenging. This requires further investigation in future prospective cohort studies. [ABSTRACT FROM AUTHOR]

Background: Malignant tumours seriously threaten human life and health, and effective treatments for cancer are still being explored. The ability of SHC SH2 domain-binding protein 1 (SHCBP1) to induce cell cycle disturbance and inhibit tumour growth has been increasingly studied, but its dynamic role in the tumour cell cycle and corresponding effects leading to mitotic catastrophe and DNA damage have rarely been studied. Results: In this paper, we found that the nucleoprotein SHCBP1 exhibits dynamic spatiotemporal expression during the tumour cell cycle, and SHCBP1 knockdown slowed cell cycle progression by inducing spindle disorder, as reflected by premature mitotic entry and multipolar spindle formation. This dysfunction was caused by G2/M checkpoint impairment mediated by downregulated WEE1 kinase and NEK7 (a member of the mammalian NIMA-related kinase family) expression and upregulated centromere/kinetochore protein Zeste White 10 (ZW10) expression. Moreover, both in vivo and in vitro experiments confirmed the significant inhibitory effects of SHCBP1 knockdown on tumour growth. Based on these findings, SHCBP1 knockdown in combination with low-dose DNA-damaging agents had synergistic tumouricidal effects on tumour cells. In response to this treatment, tumour cells were forced into the mitotic phase with considerable unrepaired DNA lesions, inducing mitotic catastrophe. These synergistic effects were attributed not only to the abrogation of the G2/M checkpoint and disrupted spindle function but also to the impairment of the DNA damage repair system, as demonstrated by mass spectrometry-based proteomic and western blotting analyses. Consistently, patients with low SHCBP1 expression in tumour tissue were more sensitive to radiotherapy. However, SHCBP1 knockdown combined with tubulin-toxic drugs weakened the killing effect of the drugs on tumour cells, which may guide the choice of chemotherapeutic agents in clinical practice. Conclusion: In summary, we elucidated the role of the nucleoprotein SHCBP1 in tumour cell cycle progression and described a novel mechanism by which SHCBP1 regulates tumour progression and through which targeting SHCBP1 increases sensitivity to DNA-damaging agent therapy, indicating its potential as a cancer treatment. [ABSTRACT FROM AUTHOR]

The residue of chestnut processing generates a large amount of waste material, a resource not adequately exploited. The antioxidant and antitumoral properties of cold and hot water extracts from discarded pericarp of four chestnut Sardinian accessions and one marron variety were studied. The antioxidant capacity of the extracts was determined by spectrophotometric and electrochemical tests. The 1,1-diphenyl-2-pic-rylhydrazyl (DPPH) and 2,2′-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) results were highly correlated with each other; likewise, a good correlation was found between Ferric Reducing Antioxidant Power (FRAP) and cyclic voltammetry (CV) values, both based on the direct transfer of electrons. The antiproliferative effect on normal cells (fibroblasts), and on colon (RKO and SW48) and breast (MCF7) cancer cells was evaluated. Additionally, this paper marks the first application of chestnut extracts to investigate their effects on melanoma (B16F10) cells. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test demonstrated that temperature and different extraction times significantly influenced the growth of cells, both normal and tumor. The fibroblast growth was significantly inhibited by moderate doses of cold extracts, while the GI50 values calculated for hot extracts were high, regardless of the accession or cultivar. An even more marked inhibitory action of the cold extracts was observed both on the growth of RKO and SW48 cells and on B16F10 melanoma cells. Otherwise, an extract concentration, both cold and hot, of no less than 243 µg mL−1 is required to achieve a 50% inhibition of MCF7 cell growth. [ABSTRACT FROM AUTHOR]

Our previous studies have introduced osteoclasts (OCs) as major activators of NK cells. It was found that OCs exhibit the capabilities of inducing cell expansion as well as increasing the cytotoxic activity of NK cells by granule release and increasing the secretion of TNF-α and TRAIL, leading to increased lysis of tumors in short-term as well as long-term periods, respectively. OC- induced expanded NK cells were named supercharged NK cells (sNK) due to their significantly high functional activity as well as their significantly higher cell expansion rate. It is, however, unclear whether the OC-mediated effect in NK cells is specific or whether other cytotoxic immune cells can also be expanded and activated by OCs. We chose to focus on γδ T cells and pan T cells, which also include CD8+ T cells. In this paper, we report that OCs are capable of expanding and functionally activating both γδ T cells and pan T cells. Expanded γδ T and pan T cells were capable of secreting high levels of INF-γ, albeit with different dynamics to those of NK cells, and, moreover, they are unable to kill NK-specific targets. Since we used humanized-BLT (hu-BLT) mice as a model of human disease, we next determined whether NK and T cell activation through OCs is also evident in cells obtained from hu-BLT mice. Similar to humans, OCs were capable of increasing the cell expansion and secretion of IFN-γ in the culture of either NK or T cells from hu-BLT mice, providing yet further evidence that these mice are appropriate models to study human disease. Therefore, these studies indicated that CD3+ T or γδ T cells can proliferate and be supercharged by OCs similar to the NK cells; thus, they can be used individually or in combination in the cell therapy of cancers. [ABSTRACT FROM AUTHOR]

Cannabinoids have incited scientific interest in different conditions, including malignancy, due to increased exposure to cannabis. Furthermore, cannabinoids are increasingly used to alleviate cancer-related symptoms. This review paper aims to clarify the recent findings on the relationship between cannabinoids and oral cancer, focusing on the molecular mechanisms that could link cannabinoids with oral cancer pathogenesis. In addition, we provide an overview of the current and future perspectives on the management of oral cancer patients using cannabinoid compounds. Epidemiological data on cannabis use and oral cancer development are conflicting. However, in vitro studies assessing the effects of cannabinoids on oral cancer cells have unveiled promising anti-cancer features, including apoptosis and inhibition of cell proliferation. Downregulation of various signaling pathways with anti-cancer effects has been identified in experimental models of oral cancer cells exposed to cannabinoids. Furthermore, in some countries, several synthetic or phytocannabinoids have been approved as medical adjuvants for the management of cancer patients undergoing chemoradiotherapy. Cannabinoids may improve overall well-being by relieving anxiety, depression, pain, and nausea. In conclusion, the link between cannabinoid compounds and oral cancer is complex, and further research is necessary to elucidate the potential risks or their protective impact on oral cancer. [ABSTRACT FROM AUTHOR]

Primary cell lines are invaluable for exploring cancer biology and investigating novel treatments. Despite their numerous advantages, primary cultures are laborious to obtain and maintain in culture. Hence, established cell lines are still more common. This study aimed to evaluate a range of techniques for isolating primary breast cancer cultures, employing distinct enzymatic compositions, incubation durations, and mechanical approaches, including filtration. Out of several protocols, we opted for a highly effective method (Method 5) that gave rise to a primary cell culture (BC160). This method combines mechanical disaggregation and enzymatic digestion with hyaluronidase and collagenase. Moreover, the paper addresses common issues in isolating primary cultures, shedding light on the struggle against fibroblasts overgrowing cancer cell populations. To make primary cell lines a preferred model, it is essential to elaborate and categorise isolation methods, develop approaches to separate heterogeneous cultures and investigate factors influencing the establishment of primary cell lines. [ABSTRACT FROM AUTHOR]

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The aim of the study was to achieve effective colon anticancer immunotherapy using the alkaloid berberine. In the presented paper we attempt to develop a formulation of berberine loaded into liposomal carriers using the vitamin C gradient method, characterized by efficient drug encapsulation, high stability during long-term storage, low drug release in human plasma with specific cytotoxicity towards colon cancer cells. Liposomal berberine was responsible for the induction of oxidative stress, the presence of Ca2+ ions in the cytosol, the reduction of Δψm, and ATP depletion with a simultaneous lack of caspase activity. Moreover, treatment with liposomal berberine led to CRT exposure on the surface of cancer cells, extracellular ATP, and HMGB1 release. The above-described mechanism of action was most likely associated with ICD induction, contributing to the increased number of phagocytic cancer cells. We have shown that cancer cells treated with liposomal berberine were phagocytosed more frequently by macrophages compared to the untreated cancer cells. What is more, we have shown that macrophage pre-treatment with liposomal berberine led to a 3-fold change in the number of phagocytosed SW620 cancer cells. The obtained results provide new insights into the role of berberine in maintaining the immune response against colorectal cancer. [ABSTRACT FROM AUTHOR]

Increased glycolysis is a key characteristic of malignant cells that contributes to their high proliferation rates and ability to develop drug resistance. The glycolysis rate-limiting enzyme hexokinase II (HK II) is overexpressed in most tumor cells and significantly affects tumor development. This paper examines the structure of HK II and the specific biological factors that influence its role in tumor development, as well as the potential of HK II inhibitors in antitumor therapy. Furthermore, we identify and discuss the inhibitors of HK II that have been reported in the literature. [ABSTRACT FROM AUTHOR]

The article titled "The Enhanced Cytotoxic and Pro-Apoptotic Effects of Optimized Simvastatin-Loaded Emulsomes on MCF-7 Breast Cancer Cells" has been retracted by the journal Pharmaceutics. Concerns were raised about image issues in the publication, and an investigation confirmed the presence of figures that had been previously published in other papers. The authors were unable to provide satisfactory explanations for the similarities in the figures, and as a result, the Editorial Board and Editor-in-Chief decided to retract the paper. It is important to note that the authors did not agree with this retraction. [Extracted from the article]

A novel NIR probe based on oxazolonaphthoimidazo[1,2- a ]pyridine-malononitrile (ONIM) conjugate linked by vinyl linkage was designed and synthesized for the detection of cyanide ion. [Display omitted] • An orange emitting sensor ONIM (712 nm) with D-π-A framework is synthesized. • The ONIM emission is retained in the solid state. • ONIM could sense cyanide ion without interference of other anions. • Sensing mechanism of cyanide sensing was confirmed by 1H NMR and DFT calculations. • Live cell imaging in human breast cancer cell MDA-MB 231 and as solid state sensor was achieved. Cyanide is undoubtedly dangerous and fast acting chemical employed in various industrial applications with toxic side effects, which raises urgent need for its monitoring. In this context, oxazolonaphthoimidazo[1,2- a ]pyridine-malononitrile (ONIM) conjugate linked by vinyl linkage was designed, synthesized and characterised by FT-IR, NMR and mass spectrometry. The developed probe has been evaluated for the colorimetric and fluorometric detection of cyanide ion. An obvious color change with unique rapid " turn-off " fluorometric response was observed within 5 s upon addition of CN– thus reflecting its better acuteness and sensitivity over other competing anions. The developed probe exhibits a detection limit of 9.54 nM which is very low in comparison to maximum permitable amount of cyanide in drinking water (1.9 µM). The probe is stable within the p H range of 2–9 and suitable for the recognition of CN– in the p H range of 7 to 10, specially at neutral p H conditions. The chemodosimetric approach based detection mechanism was authenticated by 1H NMR titration and DFT calculations. The solid state applications were established by utilising ONIM impregnated TLC plates and filter paper in cyanide recognition. The solid state emissive behaviour of ONIM offers on-spot detection of the cyanide anion. Additionally, the practicability of ONIM has been extended in live cell imaging of CN– in human breast cancer cell (MDA-MB-231), which revealed a " turn-off " fluorescence response for the probe in the presence of CN– ion. [ABSTRACT FROM AUTHOR]

The advent of cancer immunotherapy has imparted a transformative impact on cancer treatment paradigms by harnessing the power of the immune system. However, the challenge of practical and precise targeting of malignant cells persists. To address this, engineered nanoparticles (NPs) have emerged as a promising solution for enhancing targeted drug delivery in immunotherapeutic interventions, owing to their small size, low immunogenicity, and ease of surface modification. This comprehensive review delves into contemporary research at the nexus of NP engineering and immunotherapy, encompassing an extensive spectrum of NP morphologies and strategies tailored toward optimizing tumor targeting and augmenting therapeutic effectiveness. Moreover, it underscores the mechanisms that NPs leverage to bypass the numerous obstacles encountered in immunotherapeutic regimens and probes into the combined potential of NPs when co-administered with both established and novel immunotherapeutic modalities. Finally, the review evaluates the existing limitations of NPs as drug delivery platforms in immunotherapy, which could shape the path for future advancements in this promising field. This paper reviews recent advances in various nanoparticle-enhanced tumor immunotherapy strategies as delivery vehicles for immune agents. [Display omitted] [ABSTRACT FROM AUTHOR]

The article raises concerns over the scientific validity of a paper on Ribophorin II's effects on esophageal cancer, citing potential image duplication from a previous study.

The current medical standard for setting an oral cancer (OC) diagnosis is histological examination of a tissue sample taken from the oral cavity. This process is time-consuming and more invasive than an alternative approach of acquiring a brush sample followed by cytological analysis. Using a microscope, skilled cytotechnologists are able to detect changes due to malignancy; however, introducing this approach into clinical routine is associated with challenges such as a lack of resources and experts. To design a trustworthy OC detection system that can assist cytotechnologists, we are interested in deep learning based methods that can reliably detect cancer, given only per-patient labels (thereby minimizing annotation bias), and also provide information regarding which cells are most relevant for the diagnosis (thereby enabling supervision and understanding). In this study, we perform a comparison of two approaches suitable for OC detection and interpretation: (i) conventional single instance learning (SIL) approach and (ii) a modern multiple instance learning (MIL) method. To facilitate systematic evaluation of the considered approaches, we, in addition to a real OC dataset with patient-level ground truth annotations, also introduce a synthetic dataset—PAP-QMNIST. This dataset shares several properties of OC data, such as image size and large and varied number of instances per bag, and may therefore act as a proxy model of a real OC dataset, while, in contrast to OC data, it offers reliable per-instance ground truth, as defined by design. PAP-QMNIST has the additional advantage of being visually interpretable for non-experts, which simplifies analysis of the behavior of methods. For both OC and PAP-QMNIST data, we evaluate performance of the methods utilizing three different neural network architectures. Our study indicates, somewhat surprisingly, that on both synthetic and real data, the performance of the SIL approach is better or equal to the performance of the MIL approach. Visual examination by cytotechnologist indicates that the methods manage to identify cells which deviate from normality, including malignant cells as well as those suspicious for dysplasia. We share the code as open source. [ABSTRACT FROM AUTHOR]

This document is an editorial published in the journal Frontiers in Immunology. It discusses the role of Epstein-Barr virus (EBV) in inducing T cell immunity in cancers. The editorial highlights the complexity of the immune response to EBV and its significance in cancer progression and management. It also explores the potential of EBV-specific T cell responses for therapeutic purposes, including targeting EBV-associated malignancies and redirecting T cell activity to EBV-unrelated cancers. The document emphasizes the need for further research to fully understand the role of EBV-induced TAA-specific T cells in cancers not traditionally linked to the virus. [Extracted from the article]

Abstract Understand the dynamics of cancer stem cells (CSCs), prevent the non-recurrence of cancers and develop therapeutic strategies to destroy both cancer cells and CSCs remain a challenge topic. In this paper, we study both analytically and numerically the dynamics of CSCs under radiotherapy effects. The dynamical model takes into account the diffusion of cells, the de-differentiation (or plasticity) mechanism of differentiated cancer cells (DCs) and the time delay on the interaction between microRNAs molecules (microRNAs) with DCs. The stability of the model system is studied by using a Hopf bifurcation analysis. We mainly investigate on the critical time delay $$\tau _{c}$$ τ c , that represents the time for DCs to transform into CSCs after the interaction of microRNAs with DCs. Using the system parameters, we calculate the value of $$\tau _{c}$$ τ c for prostate, lung and breast cancers. To confirm the analytical predictions, the numerical simulations are performed and show the formation of spatiotemporal circular patterns. Such patterns have been found as promising diagnostic and therapeutic value in management of cancer and various diseases. The radiotherapy is applied in the particular case of prostate model. We calculate the optimum dose of radiation and determine the probability of avoiding local cancer recurrence after radiotherapy treatment. We find numerically a complete eradication of patterns when the radiotherapy is applied before a time $$t < \tau _{c}$$ t < τ c . This scenario induces microRNAs to act as suppressors as experimentally observed in prostate cancer. The results obtained in this paper will provide a better concept for the clinicians and oncologists to understand the complex dynamics of CSCs and to design more efficacious therapeutic strategies to prevent the non-recurrence of cancers.

Metal sulfide nanoparticles are synthesized for their biomedical applications, including cancer drug targeting. This paper reports a novel nanocomposite made of praseodymium sulfide nanoparticles and poly-cyclodextrin. The praseodymium sulfide nanoparticles were synthesized hydrothermal, autoclaving the nitrate precursors at 150 °C for 18 hours. The material is characterized using XRD and shows an orthorhombic crystal system with high crystallinity. The size and morphology of the nanomaterial were optimized. The material shows a rod-shaped morphology, as seen in the TEM image, with 150 ± 3 nm length and 25 ± 5 nm width. Particle size analysis supports this size range. The colloidal particles were stable in the aqueous medium without precipitation at neutral pH. The elements in the material in the polymer-coated form and their electronic states are studied by X-ray photoelectron spectroscopy. Thermogravimetry confirms that the material contains about 18.5% of the weight of the polymer. The material has an observable magnetic property at room temperature due to the praseodymium element. The UV–vis–NIR absorption spectrum of the material shows a long absorption range that extends to 1200 nm. The drug 5-fluorouracil is encapsulated in the nanoparticles through host: guest association, and its release profile is analyzed. The release is modulated at a slightly acidic pH, indicating the pH-tunability. The nanoparticles and 5-fluorouracil were taken in the w/w ratio of 2:1 (2/1 mg in 1 mL of deionized water). Further, the in vitro anticancer activity of the drug-encapsulated material is screened on breast cancer and non-cancerous cell lines. The IC 50 values are reported, and the advantageous properties of the material as drug carriers are discussed. • Drug carrier nanorods are designed using praseodymium sulfide and poly-cyclodextrin. • The nanoparticles are weakly magnetic with low saturation. • It shows a long tail absorption band that extends up to the NIR-II wavelength range. • The encapsulated 5-fluorouracil is released continually for more than 10 days. • Drug-containing Pr2S3 nanoparticles are selectively active on MCF-7 cell lines. [ABSTRACT FROM AUTHOR]

This paper focuses on the synthesis of nano-oxali-palladium coated with turmeric extract (PdNPs) using a green chemistry technique based on the reduction in the Pd (II) complex by phytochemicals inherent in turmeric extract. PdNPs were examined and characterized using Field Emission Scanning Electron Microscopy (FESEM), Dynamic Light Scattering (DLS), Fourier Transform Infrared (FTIR), and Atomic Force Microscopy (AFM). Using different spectroscopic and molecular dynamics simulations, a protein-binding analysis of the produced nanoparticle was conducted by observing its interaction with human serum albumin (HSA). Lastly, the cytotoxic effects and apoptotic processes of PdNPs were studied against the HCT116 human colorectal cell line using the MTT assay and flow cytometry tests. According to the findings, PdNPs with spherical and homogenous morphology and a size smaller than 100 nm were generated. In addition, they can induce apoptosis in colorectal cancer cells in a dose-dependent manner with a lower Cc50 (78 µL) than cisplatin and free oxali-palladium against HCT116 cells. The thermodynamic characteristics of protein binding of nanoparticles with HSA demonstrated that PdNPs had a great capacity for quenching and interacting with HSA through hydrophobic forces. In addition, molecular dynamics simulations revealed that free oxali-palladium and PdNP attach to the same area of HSA via non-covalent interactions. It is conceivable to indicate that the synthesized PdNPs are a potential candidate for the construction of novel, nature-based anticancer treatments with fewer side effects and a high level of eco-friendliness. [ABSTRACT FROM AUTHOR]

The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. It has been noted that Figure 2C MDA-MB-231 GAPDH panel appears as Figure 4A EFM-192A PI3K panel, and Figure 2C MDA-MB-231 Cyclin B1 panel appears as Figure 4A MDA-MB-231 p-PI3K panel, both with vertical flipping and stretching transformation. Additionally, the Editorial Office has concerns surrounding similarities in Figure 2CMDA-MB-231 p21 panel and Figure 4AMDA-MB-231 p-Akt panel. The authors were contacted regarding these concerns, and have offered explanations for the duplications between Figure 2C GAPDH and Figure 4A PI3K panels, as well as Figure 2C Cyclin B1 and Figure 4A p-PI3K panels. The authors state that due to mislabelling of files, similar images were accidentally used during figure assembly. However, the authors state Figure 2C p21 panel and Figure 4A p-Akt panel are from two independent experiments. The authors have provided replacement data for Figure 2C MDA-MB-231 GAPDH, Figure 2C MDA-MB-231 Cyclin B1, Figure 2C MDA-MB-231 p21, Figure 4A EFM-192A PI3K, Figure 4A MDA-MB-231 p-PI3K, and Figure 4A MDA-MB-231 p-Akt panels. However given the extent of the similarities identified between the figures, the Editorial Office is issuing an expression of concern. [ABSTRACT FROM AUTHOR]

This article, published in Oncology Letters, has been retracted due to concerns about the data presented. A reader noticed that the data in Figure 3C of the article were very similar to data that had already been published in a different article by different authors. Since the contentious data had been published prior to the submission of this article, the editor decided to retract it. The authors were asked for an explanation but did not respond. The editor apologizes for any inconvenience caused. [Extracted from the article]

This article, titled "[Retracted] Long non-coding RNA receptor activator of nuclear factor-κB ligand promotes cisplatin resistance in non-small cell lung cancer cells," was published in the journal Experimental & Therapeutic Medicine. However, it has since been retracted due to concerns raised by a reader. The reader pointed out that the data presented in Figure 4E of the article were similar to data that had already been published in a different article by different authors. The authors were asked for an explanation but did not respond. The editor has apologized for any inconvenience caused. [Extracted from the article]