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This article is an interview with Tiffany Roach and Kari Lenhart, researchers at Drexel University, about their study on the effects of stress on germ stem cells in Drosophila. They found that repeated mating stress induces reversible changes in the germ stem cell niche. The researchers also discuss their future plans to study the effects of stress on other stem cell niches and collaborate with scientists working in different organisms. Overall, their work provides insights into the impact of stress on stem cell populations. [Extracted from the article]

Atractylodin is one of the main active ingredients of Atractylodis Rhizoma. It has various pharmacological properties, such as antigastric ulcer, immune regulation, antibacterial, anti-inflammatory, antitumor, anti-oxidant, and neuroprotective properties. In the past few decades, atractylodin has attracted the attention of researchers due to its excellent therapeutic effects. This paper aims to review the pharmacology of atractylodin, focusing mainly on its pharmacological effects in tumor treatment. Atractylodin exerts its antitumor effect by regulating different signaling pathways to induce important biological events such as apoptosis, cell cycle arrest, and autophagy, inhibiting cancer cell invasion and metastasis. In the process of cell apoptosis, atractylodin mainly induces cancer cell apoptosis by downregulating the Notch signaling pathway, affecting multiple upstream and downstream targets. In addition, atractylodin induces autophagy in cancer cells by regulating various signaling pathways such as PI3K/AKT/mTOR, p38MAPK, and hypothalamic Sirt1 and p-AMPK. Atractylodin effectively induces G1/M and G2/M phase arrest under the action of multiple signaling pathways. Among them, the pathways related to G1/M are more widely stagnated. In inhibiting the migration and invasion of cancer cells, atractylodin mainly regulates the Wnt signaling pathway, downregulates the expression of N-cadherin in cancer cells, and then blocks the PI3K/AKT/mTOR signaling pathway, inhibiting the phosphorylation of PI3K, AKT, and mTOR proteins, thereby having a significant impact on the invasion and migration of cancer cells. This paper systematically reviews the research progress on the antitumor effects and mechanisms of atractylodin, hoping to provide a reference and theoretical basis for its clinical application and new drug development. [ABSTRACT FROM AUTHOR]

Intermediate filaments are one of three polymeric structures that form the cytoskeleton of epithelial cells. In the epithelium, these filaments are made up of a variety of keratin proteins. Intermediate filaments complete a wide range of functions in keratinocytes, including maintaining cell structure, cell growth, cell proliferation, cell migration, and more. Given that these functions are intimately associated with the carcinogenic process, and that hyperkeratinization is a quintessential feature of oral leukoplakias, the utility of keratins in oral leukoplakia is yet to be fully explored. This scoping review aims to outline the current knowledge founded on original studies on human tissues regarding the expression and utility of keratins as diagnostic, prognostic, and predictive biomarkers in oral leukoplakias. After using a search strategy developed for several scientific databases, namely, PubMed, Scopus, Web of Science, and OVID, 42 papers met the inclusion and exclusion criteria. One more article was added when it was identified through manually searching the list of references. The included papers were published between 1989 and 2024. Keratins 1–20 were investigated in the 43 included studies, and their expression was assessed in oral leukoplakia and dysplasia cases. Only five studies investigated the prognostic role of keratins in relation to malignant transformation. No studies evaluated keratins as a diagnostic adjunct or predictive tool. Evidence supports the idea that dysplasia disrupts the terminal differentiation pathway of primary keratins. Gain of keratin 17 expression and loss of keratin 13 were significantly observed in differentiated epithelial dysplasia. Also, the keratin 19 extension into suprabasal cells has been associated with the evolving features of dysplasia. The loss of keratin1/keratin 10 has been significantly associated with high-grade dysplasia. The prognostic value of cytokeratins has shown conflicting results, and further studies are required to ascertain their role in predicting the malignant transformation of oral leukoplakia. [ABSTRACT FROM AUTHOR]

Migrating cells in tissues are often known to exhibit collective swirling movements. In this paper, we develop an active vertex model with polarity dynamics based on contact inhibition of locomotion (CIL). We show that under this dynamics, the cells form steady-state vortices in velocity, polarity, and cell stress with length scales that depend on polarity alignment rate (ζ), self-motility (v0), and cell-cell bond tension (λ). When the ratio λ/v0 becomes larger, the tissue reaches a near jamming state because of the inability of the cells to exchange their neighbors, and the length scale associated with tissue kinematics increases. A deeper examination of this jammed state provides insights into the mechanism of sustained swirl formation under CIL rule that is governed by the feedback between cell polarities and deformations. To gain additional understanding of how active forcing governed by CIL dynamics leads to large-scale tissue dynamics, we systematically coarse-grain cell stress, polarity, and motility and show that the tissue remains polar even on larger length scales. Overall, we explore the origin of swirling patterns during collective cell migration and obtain a connection between cell-level dynamics and large-scale cellular flow patterns observed in epithelial monolayers. [ABSTRACT FROM AUTHOR]

This paper presents the findings of a comprehensive study exploring the synergistic effects arising from the combination of microwave ablation and pulsed electromagnetic field (PEMF) therapy on prostate cancer cells. The research encompassed five distinct experimental groups, with continuous electric field measurements conducted during the entire treatment process. Group 1 and Group 2, subjected to microwave power below 350 W, exhibited specific electric field values of 72,800 V/m and 56,600 V/m, respectively. In contrast, Group 3 and Group 4, exposed to 80 W microwave power, displayed electric field levels of approximately 1450 V/m, while remaining free from any observable electrical discharges. The migratory and invasive capacities of PC3 cells were assessed through a scratch test in all groups. Notably, cells in Group 3 and Group 4, subjected to the combined treatment of microwave ablation and PEMF, demonstrated significantly accelerated migration in comparison to those in Groups 1 and 2. Additionally, Group 5 cells, receiving PEMF treatment in isolation, exhibited decreased migratory ability. These results strongly suggest that the combined approach of microwave ablation and PEMF holds promise as a potential therapeutic intervention for prostate cancer, as it effectively reduced cell viability, induced apoptosis, and impeded migration ability in PC3 cells. Moreover, the isolated use of PEMF demonstrated potential in limiting migratory capacity, which could hold critical implications in the fight against cancer metastasis. In this study, a new approach to treat prostate cancer by combining microwave ablation (MWA) and pulsed electromagnetic field (PEMF) therapy is explored. We used specific devices like rectangular waveguides for MWA and circular coils for PEMF. The energy sources utilized in the study comprised a magnetron tube system, similar to the microwave source found in a microwave oven, for generating microwaves, and a signal generator for producing PEMF. We used specialized equipment for MWA and PEMF to maintain controlled conditions, ensuring precise and reliable results. The research included testing various groups of prostate cancer cells exposed to different intensities of microwave power and magnetic flux density. The movement of cancer cells in different groups was examined through a wound healing assay, where cancer cells were placed on a flat surface, and we observed whether they filled the gap created by their movement. Interestingly, cells treated with both MWA and PEMF demonstrated faster movement compared to cells treated with MWA alone or PEMF alone. This combined treatment not only effectively decreased cell movement but also showed the potential cell death. The results showed that the combination of MWA and PEMF suggest a promising therapeutic strategy. The findings contribute to the development of precise and effective therapies that could enhance patient outcomes and quality of life. However, further research and validation are essential before translating these findings into clinical applications. [ABSTRACT FROM AUTHOR]

Hyaluronic acid (HA), as one of the main components of the extracellular matrix (ECM), plays an important role in the process of wound-healing and tissue-repair processes due to its unique properties and different physiological functions. HA has an ability to maintain a moist environment that promotes healing, the stimulation of growth factors and cellular constituents, and the migration of various cells essential for healing. This paper offers a review of HA use in the process of wound healing, with emphasis on hard-to-heal wounds, and examines its various applications in ophthalmology and otorhinolaryngology. It proves HA to be a versatile agent which finds its use in various fields of medicine for its antioxidant, anti-inflammatory, antibacterial properties and accelerated wound healing. [ABSTRACT FROM AUTHOR]

Cell migration is known to be a fundamental biological process, playing an essential role in development, homeostasis, and diseases. This paper introduces a cell tracking algorithm named HFM-Tracker (Hybrid Feature Matching Tracker) that automatically identifies cell migration behaviours in consecutive images. It combines Contour Attention (CA) and Adaptive Confusion Matrix (ACM) modules to accurately capture cell contours in each image and track the dynamic behaviors of migrating cells in the field of view. Cells are firstly located and identified via the CA module-based cell detection network, and then associated and tracked via a cell tracking algorithm employing a hybrid feature-matching strategy. This proposed HFM-Tracker exhibits superiorities in cell detection and tracking, achieving 75% in MOTA (Multiple Object Tracking Accuracy) and 65% in IDF1 (ID F1 score). It provides quantitative analysis of the cell morphology and migration features, which could further help in understanding the complicated and diverse cell migration processes. [ABSTRACT FROM AUTHOR]

Cell-cell adhesion is one the most fundamental mechanisms regulating collective cell migration during tissue development, homeostasis, and repair, allowing cell populations to selforganize and eventually form and maintain complex tissue shapes. Cells interact with each other via the formation of protrusions or filopodia and they adhere to other cells through binding of cell surface proteins. The resulting adhesive forces are then related to cell size and shape and, often, continuum models represent them by nonlocal attractive interactions. In this paper, we present a new continuum model of cell-cell adhesion which can be derived from a general nonlocal model in the limit of short-range interactions. This new model is local, resembling a system of thin-film type equations, with the various model parameters playing the role of surface tensions between different cell populations. Numerical simulations in one and two dimensions reveal that the local model maintains the diversity of cell sorting patterns observed both in experiments and in previously used nonlocal models. In addition, it also has the advantage of having explicit stationary solutions, which provides a direct link between the model parameters and the differential adhesion hypothesis. [ABSTRACT FROM AUTHOR]

Dendritic cells (DCs) are specialized antigen-presenting cells that are crucial for maintaining self-tolerance, initiating immune responses against pathogens, and patrolling body compartments. Despite promising aspects, DC-based immunotherapy faces challenges that include limited availability, immune escape in tumors, immunosuppression in the tumor microenvironment, and the need for effective combination therapies. A further limitation in DC-based immunotherapy is the low population of migratory DC (around 5%–10%) that migrate to lymph nodes (LNs) through afferent lymphatics depending on the LN draining site. By increasing the population of migratory DCs, DC-based immunotherapy could enhance immunotherapeutic effects on target diseases. This paper reviews the importance of DC migration and current research progress in the context of DC-based immunotherapy. [ABSTRACT FROM AUTHOR]

Background: Studies have shown that CCR7, an important inflammatory factor, can promote the proliferation and metastasis of oral squamous cell carcinoma (OSCC), but its role in the tumor microenvironment (TME) remains unclear. This paper explores the role of CCR7 in the TME of OSCC. Methods: In this work, we constructed CCR7 gene knockout mice and OSCC mouse models. Single-cell RNA sequencing (scRNA-seq) and bioinformatics were used to analyze the differences in the OSCC microenvironment between three CCR7 gene knockout mice (KO) and three wild-type mice (WT). Immunohistochemistry, immunofluorescence staining, and flow cytometry were used to analyze the expression of key genes in significantly different cell types between the KO and WT groups. An in vitro experiment was used to verify the effect of CCR7 on M2 macrophage polarization. Results: In the mouse OSCC models, the tumor growth rate in the KO group was significantly lower than that in the WT group. Eight main cell types (including tumor cells, fibroblasts, macrophages, granulocytes, T cells, endothelial cells, monocytes, and B cells) were identified by Seurat analysis. The scRNA-seq results showed that the proportion of tumor cells was lower, but the proportion of inflammatory cells was significantly higher in the KO group than in the WT group. CellPhoneDB analysis results indicated a strong interaction relationship between tumor cells and macrophages, T cells, fibroblasts, and endothelial cells. Functional enrichment results indicated that the expression level of the Dusp1 gene in the KO group was generally higher than that in the WT group in various cell types. Macrophage subclustering results indicated that the proportion of M2 macrophages in the KO group was lower than that in the WT group. In vitro experimental results showed that CCR7 can promote M2 macrophage polarization, thus promoting the proliferation, invasion and migration of OSCC cells. Conclusions: CCR7 gene knockout can significantly inhibit the growth of mouse oral squamous cell carcinoma by promoting the polarization of M2 macrophages. [ABSTRACT FROM AUTHOR]

This paper shows for the first time that co-transplantation of human olfactory ensheathing cells with neurotrophin-3 into spinal cord cysts is more effective for activation of remyelination than transplantation of cells with brain-derived neurotrophic factor and a combination of these two factors. The studied neurotrophic factors do not affect proliferation and migration of ensheathing cells in vitro. It can be concluded that the maximum improvement of motor function in rats receiving ensheathing cells with neurotrophin-3 is largely determined by activation of remyelination. [ABSTRACT FROM AUTHOR]

Simple Summary: TP is a widely utilized anticancer medication, particularly effective in treating HCC. Thorough investigation into TP's molecular mechanism in HCC treatment is crucial for precise and combination therapy. In this paper, we have unveiled a novel mechanism of TP in HCC treatment, where it inhibits tumor growth by reducing lipid accumulation. While the inhibition of P53 gene activity is commonly thought to be the reason for TP's effectiveness in treating HCC, this new mechanism serves as a significant complement to the current understanding, paving the way for innovative approaches to HCC treatment. Hepatocellular carcinoma (HCC), which is the third leading cause of cancer-related mortality in the world, presents a significant medical challenge. Triptolide (TP) has been identified as an effective therapeutic drug for HCC. However, its precise therapeutic mechanism is still unknown. Understanding the mechanism of action of TP against HCC is crucial for its implementation in the field of HCC treatment. We hypothesize that the anti-HCC actions of TP might be related to its modulation of HCC lipid metabolism given the crucial role that lipid metabolism plays in promoting the progression of HCC. In this work, we first demonstrate that, both in vitro and in vivo, TP significantly reduces lipid accumulation in HCC cells. Additionally, we notice that lipoprotein lipase (LPL) expression is markedly upregulated in HCC, and that its levels are positively connected with the disease's progression. It is interesting to note that TP dramatically reduces LPL activity, which in turn prevents HCC growth and reduces lipid accumulation. Additionally, the effect of TP on LPL is a direct correlation. These results definitely demonstrate that TP protects hepatocytes against abnormal accumulation of lipids by transcriptionally suppressing LPL, which reduces the development of HCC. This newly identified pathway provides insight into the process through which TP exerts its anti-HCC actions. [ABSTRACT FROM AUTHOR]

High-grade gliomas are considered an incurable disease. Despite all the various therapy options available, patient survival remains low, and the tumor usually returns. Tumor resistance to conventional therapy and stimulation of the migratory activity of surviving cells are the main factors that lead to recurrent tumors. When developing new treatment approaches, the effect is most often evaluated on standard and phenotypically depleted cancer cell lines. Moreover, there is much focus on the anti-proliferative effect of such therapies without considering the possible stimulation of migratory activity. In this paper, we studied how glioma cell migration changes after exposure to bi-(AID-1-T), an anti-proliferative aptamer. We investigated the effect of this aptamer on eight human glioma cell cultures (Grades III and IV) that were derived from patients' tumor tissue; the difference between primary and recurrent tumors was taken into account. Despite its strong anti-proliferative activity, bi-(AID-1-T) was shown to induce migration of recurrent tumor cells. This result shows the importance of studying the effect of therapeutic molecules on the invasive properties of glioma tumor cells in order to reduce the likelihood of inducing tumor recurrence. [ABSTRACT FROM AUTHOR]

AbstractThe expression of both lactate dehydrogenase A (LDH-A) and glucose transporter type 1 (GLUT1) is high in pancreatic, thoracic and many other types of cancer. GLUT1 is also highly expressed in endothelial cells (EC), that play an important role in tumor metastasis. We investigated the effect of inhibition of LDH-A by NHI-2 and GLUT1 by PGL14 on cellular migration, a hallmark of metastasis, in relation to changes in intracellular purine nucleotide and nicotinamide adenine dinucleotide pools in a human microvascular endothelial cell line (HMEC-1). HMEC-1 were treated with NHI-2 and PGL14 alone or in combination. Cell migration was tested by the wound healing assay. The intracellular purine nucleotides and NAD+/NADH concentrations were measured using Reversed-Phase High Performance Liquid Chromatography (RP-HPLC). Both NHI-2 at 15 µM and 45 µM and PGL14 at 10 µM and 30 µM inhibited migration by 5 to 28% while the combination led to 46% inhibition. The drugs also decreased intracellular nucleotide pools, but only 45 µM NHI-2 altered energy charge and redox status in HMEC-1 cells. Inhibitors of glycolysis attenuated migration and the energy charge of EC and support further development of LDH-A and GLUT1 inhibitors to target cancer aggressiveness and metastasis. [ABSTRACT FROM AUTHOR]

The article features an interview with Mallika Bhattacharya, the first author of a paper titled "Steroid hormone signaling synchronizes cell migration machinery, adhesion and polarity to direct collective movement." The research focuses on the timing of cell migration and how steroid hormone signaling coordinates various mechanical aspects of cell movement. Bhattacharya discusses the challenges faced during the project, including scientific failures and the impact of the COVID-19 pandemic. She also highlights the significance of the Journal of Cell Science for publishing her paper and the support it provides to early-career researchers. Bhattacharya's contact details are provided for further inquiries. [Extracted from the article]

This document is a retraction notice from the journal Bioscience Reports. The article titled "MicroRNA-223 decreases cell proliferation, migration, invasion and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O1" is being retracted due to concerns raised about the data presented in the paper. The concerns include similarities with figures from other papers, inconsistencies in the data, and the authors' lack of response to the journal's queries. The Editorial Board has made the decision to retract the article. [Extracted from the article]

The article titled "Retraction: Downregulated microRNA-30b-3p inhibits proliferation, invasion and migration of glioma cells via inactivation of the AKT signaling pathway by upregulating RECK" has been retracted by Bioscience Reports. The retraction was prompted by concerns raised by a reader regarding the appearance of Western blots in the paper, which lacked background details and resembled blots from other papers. The Editorial Team also discovered undeclared image replacements in Figures 2B, 4A, and 5B. The authors have not responded to the concerns or queries from the journal. The decision to retract the article was made by the Editorial Board. [Extracted from the article]

Thromboangiitis obliterans (TAO) is characterized by inflammation and obstruction of small-and medium-sized distal arteries, with limited pharmacotherapies and surgical interventions. The precise pathogenesis of TAO remains elusive. By utilizing the technology of tandem mass tags (TMT) for quantitative proteomics and leveraging bioinformatics tools, a comparative analysis of protein profiles was conducted between normal and TAO rats to identify key proteins driving TAO development. The results unveiled 1385 differentially expressed proteins (DEPs) in the TAO compared with the normal group-comprising 365 proteins with upregulated expression and 1020 proteins with downregulated expression. Function annotation through gene ontology indicated these DEPs mainly involved in cell adhesion, positive regulation of cell migration, and cytosol. The principal signaling pathways involved regulation of the actin cytoskeleton, vascular smooth contraction, and focal adhesion. The roles of these DEPs and associated signaling pathways serve as a fundamental framework for comprehending the mechanisms underpinning the onset and progression of TAO. Furthermore, we conducted a comprehensive evaluation of the effects of S100A8/A9 and its inhibitor, paquinimod, on smooth muscle cells (SMCs) and in TAO rats. We observed that paquinimod reduces SMCs proliferation and migration, promotes phenotype switching and alleviates vascular stenosis in TAO rats. In conclusion, our study revealed that the early activation of S100A8/A9 in the femoral artery is implicated in TAO development, targeting S100A8/A9 signaling may provide a novel approach for TAO prevention and treatment. • What is known about this topic? • TAO is characterized by inflammation and obstruction of small-and medium-sized distal arteries with limited pharmacotherapies and surgical interventions. • Identification of the protein profiles in the thromboangiitis obliterans group showed qualitative and quantitative changes. • The mechanisms underlying the phenotypic transition of SMCs in TAO remain unclear. • What does this paper add? • A total of 1385 differentially expressed proteins were identified in the TAO compared with sham group, including 365 up-regulated and 1020 down-regulated proteins. • The early activation of S100A8/A9 is implicated in TAO development, which may be a potential biomarker. Targeting S100A8/A9 signaling may provide a novel approach for TAO prevention and treatment. [ABSTRACT FROM AUTHOR]

Cellular contractility, migration, and extracellular matrix (ECM) mechanics are critical for a wide range of biological processes including embryonic development, wound healing, tissue morphogenesis, and regeneration. Even though the distinct response of cells near the tissue periphery has been previously observed in cell-laden microtissues, including faster kinetics and more prominent cell-ECM interactions, there are currently no models that can fully combine coupled surface and bulk mechanics and kinetics to recapitulate the morphogenic response of these constructs. Mailand et al. (Biophys J 117(5):975–986, 2019) had shown the importance of active elastocapillarity in cell-laden microtissues, but modeling the distinct mechanosensitive migration of cells on the periphery and the interior of highly deforming tissues has not been possible thus far, especially in the presence of active elastocapillary effects. This paper presents a framework for understanding the interplay between cellular contractility, migration, and ECM mechanics in dynamically morphing soft tissues accounting for distinct cellular responses in the bulk and the surface of tissues. The major novelty of this approach is that it enables modeling the distinct migratory and contractile response of cells residing on the tissue surface and the bulk, where concurrently the morphing soft tissues undergo large deformations driven by cell contractility. Additionally, the simulation results capture the changes in shape and cell concentration for wounded and intact microtissues, enabling the interpretation of experimental data. The numerical procedure that accounts for mechanosensitive stress generation, large deformations, diffusive migration in the bulk and a distinct mechanism for diffusive migration on deforming surfaces is inspired from recent work on bulk and surface poroelasticity of hydrogels involving elastocapillary effects, but in this work, a two-field weak form is proposed and is able to alleviate numerical instabilities that were observed in the original method that utilized a three-field mixed finite element formulation. [ABSTRACT FROM AUTHOR]

Dielectrophoresis has been widely applied in microfluidic cell separation, and it enables label-free and size-independent cell sorting based on their dielectric fingerprints which is prerequisite for downstream biomedical analysis. The linear flow velocity and cross-sectional area are the two key factors proportional to the flow rate and thus directly related to the sample processing throughput. Aiming at higher flow rate, the state-of-art techniques mostly focus on the cross-sectional area, either by using wide chamber with angled electrode digits or 3D volumetric electrodes with expanded channel depth. On the other hand, the velocity is always carefully limited because cells have very squeezed time to interact with the DEP force that drives them to migrate, and the flow drag induced by high velocity potentially poses adverse effect against the DEP-driven cell migration. In this paper, we present DEP-activated cell sorting at high-velocity being 1–2 orders of magnitude higher than the existing DEP separators, which is enabled by easily-fabricated two-layer 3D sidewall electrodes extending along the entire flow channel. Such electrodes project DEP force fully decoupled from the flow drag, and acting on cells continuously, allowing sufficient time for cell migration. The two-layer design leads to cell migration across a shorter distance between the upper and lower layers, with a unique bridge adaptor evolved at the downstream for the collection of the cells vertically separated. The DEP device achieves separation of live and dead yeast cells at high velocity up to 78.3 mm/s, more than a full order of magnitude higher compared to any reported DEP platforms. This velocity corresponds to a competitive flow rate of 3.1 mL/h given the fairly small cross-sectional area, where the averaged collection rate is over 95 %. For the separation between the live and dead Hela cells, our device enables a high velocity up to 50.5 mm/s with an averaged collection rate of ∼85 %. A high throughput of 1.79 × 1 0^(5) cells/min for the live and dead Hela cell separation has been achieved with 89.7 % collection for live cells and a velocity of 30.3 mm/s. • A unique design of two-layer electrodes extending along the entire channel. • Rapid cell lateral migration enabled by continuously exerted strong DEP force. • Fully decoupled DEP force and flow drag force, eliminating their interference. • DEP-driven cell migration from the lower to upper layer across a short distance. • High velocity up to78.3 mm/s achieved for DEP-activated cell separation [ABSTRACT FROM AUTHOR]

• Understanding the CXCR4/CXL12 axis is essential for novel melanoma treatments. • The significance of CXCR4 as a melanoma biomarker was explored. • The use of CXCR4 inhibitors to fight melanoma metastases is discussed. Melanoma is a particularly aggressive type of skin cancer that can spread to distant organs, resulting in poor patient outcomes. C-X-C motif chemokine ligand 12 (CXCL12) interacts to the C-X-C chemokine receptor type 4 (CXCR4). This connection between CXCR4 and its companion ligand CXCL12 is important in melanoma metastasis and progression, encouraging cell proliferation, invasion, and survival via downstream signaling pathways. Furthermore, CXCR4 is implicated in the interaction between melanoma cells and the tumor microenvironment, which promotes malignant cell migration and immune evasion. Given the importance of the CXCR4/CXCL12 axis in melanoma, addressing this axis has the potential to prevent metastasis and improve patient outcomes. We present an overview of the CXCR4/CXCL12 axis in cancer progression and explain its role in the melanoma microenvironment in this paper. Furthermore, we investigate CXCR4's predictive usefulness as a possible biomarker for monitoring melanoma progression. Finally, we discuss the most recent research and clinical trials on CXCR4 inhibitors, emphasizing their efficacy and limits. We hope to improve the quality of life for melanoma patients by better understanding the role of CXCR4 and investigating novel therapeutic options. [ABSTRACT FROM AUTHOR]

This article, titled "[Retracted] MicroRNA-378 regulates cell proliferation and migration by repressing RNF31 in pituitary adenoma," was published in Oncology Letters in 2018. However, it has since been retracted due to concerns raised by a reader. The reader pointed out similarities between the scratch-wound assay data in Figure 3 of this article and data from a different paper submitted to the same journal. Additionally, there were possible anomalies in the "Control" panel. The editor decided to retract the paper due to a lack of confidence in the data and the authors did not provide an explanation. [Extracted from the article]

In this paper, a heart-shaped nanocomposite (MXenen@Cu-MOF, MC) has been prepared by hydrothermal method. This material can effectively prevent the accumulation of MXene, improve the material's electrical conductivity and antibacterial properties. In addition, it is loaded into Polyvinyl alcohol/Poly-dopamine hydrogel wound dressings (PPMC), which can effectively destroy bacterial biofilms and provide a new pathway for internal electrical currents, helping to repair internal electric fields and promote wound healing. Through the concentration gradient experiments of hydrogel such as antibacterial, conductive, hemolysis and cell migration, we believe that the addition of MC can improve the basic properties of hydrogel. Among them, PPMC0.2 is the hydrogel with the best performance under the premise of meeting bio-compatibility. Its resistance, between 500 and 1000 Ω, is lower than the skin resistance at the wound site and provides the basis for the passage of current through the body. In addition, the cell mobility (24h) of PPMC0.2 reached 58%, and the wound healing rate (6day) was 81.84%, which was much higher than that of other experimental groups. The experimental results proved that PPMC hydrogel can promote wound healing, and this study also provided a new therapeutic idea for chronic wound healing. [ABSTRACT FROM AUTHOR]

It was reported that within the head and neck cancer (HNC) cell line CAL21 the epithelial-mesenchymal transition (EMT) and cell proliferation were promoted by Urokinase-Type Plasminogen Activator (PLAU) proteinase through TNFRSF12A. Additionally, in this paper HNC cell lines refer to Fadu and Tu686. A novel PLAU-STAT3 axis was found to be involved in HNC cell line proliferation and metastasis. PLAU expression in HNC samples was upregulated, besides, the elevated expression of PLAU was linked to the lower overall survival (OS) and disease-free survival (DFS). Ectopic PLAU expression promoted cell proliferation and migration, while PLAU knockdown exhibited opposite results. RNA-seq data identified the JAK-STAT signaling pathway, confirmed by western blotting. A recovery assay using S3I-201, a selective inhibitor of signal transducer and activator of transcription 3 (STAT3), indicated that PLAU promoted HNC cell line progression via STAT3 signaling in vitro. The oncogenic role of PLAU in HNC tumor growth in vivo was confirmed using xenograft models. In summary, we identified the tumorigenic PLAU function in the HNC progress. PLAU may represent a potential prognostic biomarker of HNC and the PLAU-STAT3 pathway might be considered a therapeutic target of HNC. • High PLAU expression indicates poor overall and disease-free survival of HNC. • PLAU promotes HNC cell proliferation and migration via JAK-STAT signaling pathway. • PLAU suppresses HNC tumor growth in vivo. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "The journey of a generation: advances and promises in the study of primordial germ cell migration." The correction states that there were errors in the production process, specifically with the orientation of some arrows in Figure 1A. The original and corrected figure panels are provided. The journal apologizes for any inconvenience caused and confirms that the online versions of the paper have been corrected. [Extracted from the article]

The article titled "[Retracted] miR-660-5p is associated with cell migration, invasion, proliferation and apoptosis in renal cell carcinoma" was published in Molecular Medicine Reports in 2018. The authors of the article contacted the Editorial Office to report errors in the data handling and labeling of representative images in Figures 3B and 5A. An independent investigation by the Editorial Office revealed overlapping data panels in Figures 6A and 6B, indicating a lack of confidence in the presented data. As a result, the Editor decided to retract the paper. The authors accepted this decision, and the Editor apologizes for any inconvenience caused. [Extracted from the article]

Steroid hybrids have emerged as a type of advantageous compound as they could offer improved pharmacological and pharmaceutical properties. Here, we report a series of novel peptide–dehydroepiandrosterone hybrids, which would effectively induce endoplasmic reticulum stress (ERS) and lead to apoptosis with outstanding in vitro and in vivo anti-melanoma effects. The lead compound IId among various steroids conjugated with peptides and pyridines showed effective in vivo activity in B16 xenograft mice: in medium- and high-dose treatment groups (60 and 80 mg/kg), compound IId would significantly inhibit the growth of tumours by 98%–99% compared to the control group, with the highest survival rate as well. Further mechanism studies showed that compound IId would damage the endoplasmic reticulum and upregulate the ERS markers C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78), which could further regulate caspase and Bcl-2 family proteins and lead to cell apoptosis. The compound IId was also proven to be effective in inhibiting B16 cell migration and invasion. This paper reports a series of peptide-dehydroepiandrosterone (DHEA) conjugates with the ability to damage endoplasmic reticulum and upregulate endoplasmic reticulum stress markers which finally leads to apoptosis in melanoma. The lead compound IId has IC 50 of 9.70 μM against B16 melanoma cell line and the tumour-inhibitory rate in vivo was 98% after 27 days treatment in 0.06–0.08 mg/g dose groups and also demonstrated a good dose-effect and time-effect relationship. [Display omitted] • A series of novel peptide-dehydroepiandrosterone hybrids were synthesised. • Peptidyl modifications provided dehydroepiandrosterone derivatives with the ability to suppress melanoma both in vitro and in vivo. • The lead compound IId would trigger endoplasmic reticulum stress to induce apoptosis in B16 cells. • In xenograft model, IId (60 mg/kg and 80 mg/kg groups) would inhibit the growth of tumour by 98%–99% compared to control. [ABSTRACT FROM AUTHOR]

This document is a corrigendum for an article titled "Pien Tze Huang inhibits hypoxia-induced epithelial-mesenchymal transition in human colon carcinoma cells through suppression of the HIF-1 pathway." The authors of the article realized that they had uploaded an incorrect figure for Figure 3A, which showed an overlap of data with Figure 4A. They requested a correction, and the corrected version of Figure 3, showing the correct data for the Hypoxia + PZH experiments, is provided. The authors apologize for any inconvenience caused and state that this error did not affect the overall conclusions of the paper. [Extracted from the article]

E-cadherin plays a critical role in preserving cell-cell adhesion and tissue integrity, and its reduced expression is a hallmark feature of the epithelial-mesenchymal transition (EMT) associated with cancer metastasis. This paper explores signaling pathways, including Snail family transcriptional repressor (Snail), Mitogen-activated protein kinase (MAPK), Store-operated calcium entry (SOCE), Transforming growth factor (TGF-β), Janus kinase/signal transducers and activators of transcription (JAK/STAT), Wingless-related integration site (Wnt), and Renin angiotensin system (RAS), elucidating their functions in regulating E-cadherin levels and controlling cell migration and proliferation. Also, regulation of E-cadherin signaling pathways by various dietary components is explored. This comprehensive review presents the critical role of E-cadherin and its associated pathways in various diseases, particularly cancer and cardiovascular conditions. Additionally, the article discusses the influence of dietary components like antioxidants, polyphenols, and herbs on E-cadherin pathways, offering potential pathways for modulating cell migration and proliferation in chronic diseases. It emphasizes the potential for therapeutic interventions targeting these pathways and suggests the significance of considering dietary factors in disease prevention and treatment strategies. • Loss of E-cadherin is an essential element of invasion and metastasis. • E-cadherin and related pathways including Snail, MAPK, SOCE, TGF-β, JAK/STAT, Wnt, and RAS regulate migration and proliferation. • Dietary components influence the E-cadherin pathways and interaction. [ABSTRACT FROM AUTHOR]

Snail mucus had medical applications for wound healing as early as ancient Greece and the late Han Dynasty (China). A literature search found 165 modern research papers discussing the extraction methods, chemical compositions, pharmacological activities, and applications of snail mucus. Thus, this review summarized the research progress on the extraction, structure, pharmacological activities, and applications of polysaccharides and proteins isolated from snail mucus. The extraction methods of snail mucus include natural secretion and stimulation with blunt force, spray, electricity, un-shelling, ultrasonic-assisted, and ozone-assisted. As a natural product, snail mucus mainly comprises two polysaccharides (glycosaminoglycan, dextran), seven glycoproteins (mucin, lectin), various antibacterial peptides, allantoin, glycolic acid, etc. It has pharmacological activities that encourage cell migration and proliferation, and promote angiogenesis and have antibacterial, anti-oxidative and anticancer properties. The mechanism of snail mucus' chemicals performing antibacterial and wound-healing was proposed. Snail mucus is a promising bioactive product with multiple medical applications and has great potential in the pharmaceutical and healthcare industries. Therefore, this review provides a valuable reference for researching and developing snail mucus. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] • 18 novel drug molecules of microtubulin and EGFR dual-target were prepared. • 10c showed moderate inhibition of tubulin polymerization and potent inhibition of EGFR kinase. • 10c displayed ideal tumor growth inhibition in the A549 cancer bearing nude mice models. • The balanced dual-target antitumor design could inspire the further development of single-molecule multi-target drugs. Motivated by the clinical success of combining tyrosine kinase inhibitors with microtubule-targeted drugs in antitumor treatment, this paper presents a novel combi-targeting design for dual-target inhibitors, featuring arylformylurea-coupled quinazoline backbones. A series of target compounds (10a-10r) were designed, synthesized, and characterized. Biological assessments demonstrated that 10c notably potentiated ten tumor cell lines in vitro, with IC 50 values ranging from 1.04 µM to 7.66 µM. Importantly, 10c (IC 50 = 10.66 nM) exhibited superior inhibitory activity against EGFR kinases compared to the reference drug Gefitinib (25.42 nM) and reduced phosphorylated levels of EGFR, AKT, and ERK. Moreover, 10c significantly impeded tubulin polymerization, disrupted the intracellular microtubule network in A549 cells, induced apoptosis, led to S-phase cell cycle arrest, and hindered cell migration. In anticancer evaluation tests using A549 cancer-bearing nude mice models, 10c showed a therapeutic effect similar to Gefitinib, but required only half the dosage (15 mg/kg). These findings indicate that compound 10c is a promising dual-target candidate for anticancer therapy. [ABSTRACT FROM AUTHOR]

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]

Cancer remains the primary cause of mortality in developed nations. Although localized tumors can be effectively addressed through surgery, radiotherapy, and other targeted methods, drug efficacy often wanes in the context of metastatic diseases. As a result, significant efforts are being made to develop drugs capable of not only inhibiting tumor growth but also impeding the metastasis of malignant tumors, with a focus on hindering their migration to adjacent organs. Cancer stem cells metastasize via blood and lymphatic vessels, exhibiting a high mutation rate, significant variability, and a predisposition to drug resistance. In contrast, endothelial cells, being less prone to mutation, are less likely to give rise to drug-resistant clones. Furthermore, the direct contact of circulating anti-angiogenic drugs with vascular endothelial cells expedites their therapeutic impact. Hence, anti-angiogenesis targeted therapy assumes a pivotal role in cancer treatment. This paper provides a succinct overview of the molecular mechanisms governing the interaction between cancer stem cells and angiogenesis. [ABSTRACT FROM AUTHOR]

In this study, we investigated the structural characterization and biological activities of Bletilla striata polysaccharides (BSPs) for their role as antioxidants and anti-melanogenesis agents in skin healthcare protection. Three neutral polysaccharides (BSP-1, BSP-2, and BSP-3) with molecular weights of 269.121 kDa, 57.389 kDa, and 28.153 kDa were extracted and purified. Their structural characteristics were analyzed by ion chromatography, GC–MS, and 1D/2D NMR. The results showed that BSP-1, which constitutes the major part of BSPs, was composed of α-D-Glcp, β-D-Glcp, β-D-Manp, and 2- O -acetyl-β-D-Manp, with the branched-chain accompanied by β-D-Galp and α-D-Glcp. BSP-1, BSP-2, and BSP-3 can enhance the total antioxidant capacity of skin fibroblasts with non-toxicity. Meanwhile, BSP-1, BSP-2, and BSP-3 could significantly inhibit the proliferative activity of melanoma cells. Among them, BSP-1 and BSP-2 showed more significance in anti-melanogenesis, tyrosinase inhibition activity, and cell migration inhibition. BSPs have effective antioxidant capacity and anti-melanogenesis effects, which should be further emphasized and developed as skin protection components. [Display omitted] • Three antioxidant polysaccharides (BSP-1, BSP-2, and BSP-3) were isolated from Bletilla striata. • BSPs can enhance the intracellular T-AOC of skin fibroblasts with non-toxicity. • BSPs have antiproliferative effects on B16F10 cells. • BSP-2 and BSP-3 significantly inhibit melanogenesis, tyrosinase activity and cell migration of B16F10. [ABSTRACT FROM AUTHOR]