Search

Copyright of Cancer Research on Prevention & Treatment is the property of Cancer Research on Prevention & Treatment Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer causes a significant threat to human health. Despite considerable advancements in the treatment technologies in recent years, the five-year survival rate for lung cancer patients remains low. In this context, the discovery of pyroptosis, a unique cell death mechanism, offers a novel perspective for exploring new pathways of lung cancer treatment. Particularly, the role of gasdermin E (GSDME) in the process of pyroptosis reveals its tremendous potential in lung cancer therapy. Recent studies have made considerable progress in understanding the role of GSDME-mediated pyroptosis in lung cancer growth, the lung cancer microenvironment, and the effect of GSDME methylation on lung cancer treatment. This paper summarizes these research advancements and analyzes the potential and possible side effects of GSDME-mediated pyroptosis in lung cancer therapy, aiming to provide a theoretical foundation for developing more effective strategies for lung cancer treatment. [ABSTRACT FROM AUTHOR]

The regulation of the cell cycle is essential for maintaining normal cellular function, especially in the development of diseases such as lung cancer. The cell cycle consists of four major phases (G1, S, G2 and M phases), which are characterized by a series of precise molecular events to ensure proper cell proliferation and division. In lung cancer cells, cell cycle dysregulation can lead to disordered proliferation and increased invasiveness of cancer cells. G2 and S-phase expressed 1 (GTSE1) is a regulatory protein found in the cytoplasm of the cell, which plays a key role in the cell cycle distribution of a wide range of cancer cells and is involved in life processes such as cell proliferation and apoptosis. GTSE1 affects cell cycle progression by interacting with cyclin-dependent kinase inhibitor 1A (p21) and maintaining the stability of p21, which in turn inhibits the activity of cyclin-dependent kinase 1/2 (CDK1/2). In addition, GTSE1 is also involved in the regulation of tumor protein 53 (p53) signaling pathway. With the assistance of mouse double minute 2 homolog (MDM2), GTSE1 is able to transport p53 from the nucleus to the cytoplasm and promote its ubiquitination and degradation, thus affecting cell cycle and cell deathrelated signaling pathways. This paper reviews the expression of GTSE1 in lung cancer cells and its effects on lung cancer, as well as its potential mechanisms involved in cell cycle regulation. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Arteriosclerosis is the property of Chinese Journal of Arteriosclerosis Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cancer Research on Prevention & Treatment is the property of Cancer Research on Prevention & Treatment Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Shanghai Jiaotong University (Medical Science) is the property of Journal of Shanghai Jiaotong University (Medical Science) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Programmed cell death is an important biological process, including apoptosis, autophagy and other modalities, which is essential for maintaining homeostasis of tissue and organ. In recent years, several studies have shown that aberrant regulation of programmed cell death plays an important role in the development of colorectal cancer. Therefore, it is important to reveal the fine-turned regulatory network of programmed cell death in colorectal carcinogenesis and progression to develop new clinical treatment strategies for colorectal cancer. This paper aims to review the research progress of programmed cell death in colorectal cancer, and provide new ideas and approaches for the clinical diagnosis and treatment of colorectal cancer.

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cancer cells refer to a group of malignant cells with strong division and proliferation abilities. Cancer cells rely on the unstable plunder of human nutrition to sustain the large amount of energy that they need for their own division and proliferation. The division and proliferation of cancer cells are linked to the synthesis and replication of genetic material in the nucleus. Blockage or destruction of the synthesis of genetic material in cancer cells is one of the mechanisms underlying the action of most antitumor drugs. As the key material that dominates cell division, proliferation, and death, nuclear genetic material which mainly refers to the deoxyribonucleic acid located on the chromatin in the nucleus, plays a decisive role in the final fate of cells. The final fate of cancer cells after the damage of the genetic material is worthy of investigation and analysis. In this paper, we discuss and analyze the fate of cancer cells after genetic material damage from the aspect of cellular cycle arrest, apoptosis, autophagy, and senescence to provide ideas for the mechanism research on antitumor drugs.

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Ferroptosis is a recently recognized form of regulated cell death caused by an iron-dependent accumulation of lipid reactive species. However, little research on ferroptosis and lung cancer, one of the most common tumors, has been carried out. This paper tries to review the research progress of ferroptotic suppression and explain it from the different ways of ferroptosis occurrence. Furthermore, as inducing ferroptosis to treat cancer gets more attention, we introduce four kinds of ferroptosis-inducing compounds and new prospects for lung cancer therapy to provide new ideas for lung cancer treatment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Shanghai Jiaotong University (Medical Science) is the property of Journal of Shanghai Jiaotong University (Medical Science) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Programmed cell death (PCD) is a genetically determined, active and orderly cell death in the organism, and it affects the evolution of the organism, maintenance of its homeostasis, and development of several tissues and organs. The abnormal regulation of this process is closely related to various human diseases, including cancer. The identified pathways of PCD include apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, which can be activated when cells are stimulated by various internal and external environmental factors. These pathways can induce cell death or maintain cell survival in kidney cancer cells under the regulation of various signaling molecules, thus affecting tumor progression or therapeutic efficacy. In this paper, the role of these PCD pathways in the development of kidney cancer was reviewed in light of recent research advances to provide new directions for the in-depth study of the pathogenesis of kidney cancer and the development of targeted antitumor drugs.

Serum uric acid (sUA), a natural antioxidant in human body, has been found to be related to the occurrence and development of various neurodegenerative diseases in recent years, including Parkinson's disease (PD), multiple system atrophy (MSA), Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). Increasing of sUA level has been found to reduce the incidence of PD and ALS, but the relationship between sUA and AD, MSA remains largely unknown. The in vitro studies and animal experiments revealed that sUA can enhance the antioxidant capacity of neurons and delay neurodegeneration and apoptosis. This paper mainly reviews the progress in epidemiological and basic studies of the relationship between sUA and neurodegenerative diseases in recent years, and aims to provide a reference for future novel prevention and treatment strategies for neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Objective * To explore the expression of microRNA-30b-5p (miR-30b-5p) in polycystic ovary syndrome (PCOS) rats and the effect of miR-30b-5p overexpression on ovarian granulosa cell (GC) autophagy. Methods * Dehydroepiandrosterone (DHEA) was performed to establish a PCOS rat model, and real-time fluorescent quantitative PCR (qRT-PCR) and Western blotting were performed to measure the expression of miR-30b-5p and autophagy-associated protein 5 homologue (Atg5) in the ovarian tissues of the normal group and PCOS group. Primary PCOS rat ovarian GCs were isolated and cultured, and divided into control group, miR-NC group, miR-30b-5p overexpression group, miR-30b-5p overexpression+pcDNA3.1-NC group, and miR-30b-5p overexpression+pcDNA3.1-Atg5 group. In addition, the ovarian GC of the normal group was taken as the blank group. MiR-30b-5p mimic, pcDNA3.1-Atg5 and the corresponding negative control were transfected into the cells, and 48 h after transfection, qRT-PCR was performed to measure the expression of miR-30b-5p and Atg5 mRNA of cells in each group to verify the transfection effect. CCK-8 and flow cytometer were performed to measure cell viability and apoptosis rate, respectively; immunofluorescence staining was performed to measure the positive expression of microtubule-associated protein 1 light chain 3 (LC3) in each group. Western blotting was performed to measure the protein expression of autophagy-related proteins Atg5, p62, Beclin-1 and LC3. Results * The expression level of miR-30b-5p in the ovarian tissue of the PCOS group was significantly lower than that of the normal group, and the levels of Atg5 mRNA and protein were significantly higher than those of the normal group (all P=0.000). After transfection, compared with the blank group, the miR-30b-5p level, apoptosis rate, and p62 protein level in the ovarian GC of the control group were significantly reduced, the Atg5 mRNA and protein levels, cell proliferation activity, LC3 positive cell percentage, Beclin-1 protein level and LC3H /LC3 I ratio were significantly increased (all P=0.000). Compared with the control group, the miR-30b-5p level, apoptosis rate, and p62 protein level in the ovarian GC of the miR-30b-5p overexpression group were significantly increased, and the Atg5 mRNA and protein levels, cell proliferation activity, LC3 positive cell percentage, Beclin-1 protein level and LC3H / LC31 ratio were significantly reduced (all P=0.000). Up-regulation of Atg5 can significantly attenuate the inhibitory effect of miR- 30b-5p overexpression on ovarian GC proliferation and autophagy (all P=0.000). Conclusion-MiR-30b-5p is lowly expressed in PCOS; overexpression of miR-30b-5p can inhibit the proliferation and autophagy of ovarian GC in PCOS rats, and promote cell apoptosis, and its mechanism may be related to the inhibition of Atg5 expression. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Shanghai Jiaotong University (Medical Science) is the property of Journal of Shanghai Jiaotong University (Medical Science) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of China Oncology is the property of Editorial Board of China Oncology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Shanghai Jiaotong University (Medical Science) is the property of Journal of Shanghai Jiaotong University (Medical Science) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and purpose: PRUNE2 is a specific prognostic gene for neuroblastoma and plays an important role in regulating cellular differentiation, proliferation and invasion of neuroblastoma. Low expression of PRUNE2 gene is associated with poor prognosis of prostate cancer. The aim of this paper was to investigate the correlation of PRUNE2 mutation with proliferation, apoptosis, invasion and migration of prostate cancer DU145 cells. Methods: Recombinant plasmids carrying wild-type and mutant-type PRUNE2 were constructed and then transfected to prostate cancer DU145 cell line to construct corresponding stable transgenic strains. Cell counting kit-8 (CCK-8) assay and clone formation assay were used to detect the ability of cell proliferation. Apoptosis assay was used to detect the ability of apoptosis, and transwell assay was used to detect the abilities of invasion and migration of cells. Western blot was used to detect the level of protein expression. The interaction between proteins was detected by immunofluorescence and immunoprecipitation experiments. Results: DU145 cells transfected with mutant-type PRUNE2 E370K exhibited significantly increased proliferation, invasion and migration, but significantly decreased apoptosis (P

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Oropharyngeal carcinoma is a highly heterogeneous disease that is mainly caused by tobacco and alcohol abuse or high-risk human papillomavirus (HPV) infection. HPV-positive oropharyngeal carcinoma and HPV-negative oropharyngeal carcinoma have obvious differences in etiology, epidemiology and prognosis; therefore, different methods should be adopted for treatment. It is known that the TP53 gene is not mutated in HPV-positive oropharyngeal carcinoma, and radiation therapy can activate it and induce cell apoptosis via DNA damage. There are common repair pathways to DNA damage, such as nonhomologous end joining, and this pathway is more sensitive to radiotherapy under the inhibition of HPV oncoprotein. In addition, the further activation of the immune response under the effect of radiation also participates in the elimination of tumors. In this paper, we reviewed the research on the sensitivity of HPV-positive oropharyngeal cancer to radiotherapy to provide a scientific basis for targeted treatment for various pathogenic factors and clinical stages of oropharyngeal cancer in the future.

Osteocytes, which develop from osteoblasts, are recognized as the main cells embedded in mature bone tissue. The traditional notion is that osteocytes exclusively play a structural role, however, with the development of related research in recent years, the role of osteocytes in bone metabolism has been explored. Periodontitis is a chronic inflammatory disease initiated by plaque biofilm, and is the main cause of adult tooth loss. Clinically, periodontitis primarily manifests as attachment loss, bleeding on probing and other symptoms. Alveolar bone resorption is the most characteristic pathological change. Current research demonstrated that osteocytes sense mechanical stress, participate in bone remodeling, regulate mineral balance, and participate in endocrine function. Thus, these cells play an important role in bone homeostasis and systemic metabolic balance. Osteocytes are actively involved in the development of periodontitis through the high expression of receptor activator of nuclear factor kappa B ligand (RANKL), secretion of sclerostin, and effect on apoptosis, senescence and autophagy. In the future, the detection of bone cell metabolism-related products will have certain application prospects for the clinical evaluation of periodontitis prevention and treatment. Therefore, this paper reviewed the role of osteocytes in bone homeostasis and the relationship between osteocytes and periodontitis, to provide new ideas for the prevention and treatment of periodontitis.

Lung cancer is one of the most common malignant tumors in the world, but its pathogenesis has still been remaining confusing. As an important protein in several signaling pathways, Akt has been identified to play a major role in the growth, proliferation, apoptosis and invasion of tumor cells. This paper is to review the effects of Akt, together with PDK1, Raf-1 and p70S6K, which are upstream and downstream regulatory molecules of Akt, and provide a new basis for the pathogenesis of non-small cell lung cancer. [ABSTRACT FROM AUTHOR]

Objective·To explore the inhibitory effect and its mechanism of the PDSORBS2 peptide on H9C2 cell apoptosis induced by hypoxia and reoxygenation (H/R). Methods·In the previous work of this study, a new peptide PDSORBS2 (LPASLNS) was discovered from rat cardiomyocytes after ischemia. Cell counting kit-8 (CCK-8) was used to detect cell viability to select the appropriate concentration of PDSORBS2 peptide and the appropriate time for H/R treatment. The cells were randomly divided into normal control group (NC group), NC+PDSORBS2 group, H/R group and H/R+PDSORBS2 group. A fluorescence microscope was used to observe the changes in the nucleus morphology. The degree of apoptosis and cell cycle was analyzed by flow cytometry. A kit was used to detect the content of reactive oxygen species (ROS) in cells. The expression levels of apoptosis-related proteins including poly ADP-ribose polymerase (PARP), cleaved-caspase3, B-cell lymphoma-2 (Bcl-2), and BCL2-associated X (Bax), extracellular regulated protein kinases (ERK), protein kinase B (AKT), cyclin-dependent kinases 2 (CDK2), and p27Kip1 protein were analyzed by Western blotting in H9C2 cells. Results·Compared with the NC group, 6 h of hypoxia and 2 h of reoxygenation significantly decreased the viability of H9C2 cells, while 50 µmol/L PDSORBS2 significantly increased the viability of H9C2 cells induced by H/R (P=0.004). Compared with the H/R group, the pretreatment of PDSORBS2 improved the morphology of H9C2 nuclei induced by H/R and reduced the apoptotic rate of H9C2 cells (P=0.000), cell cycle arrest (P=0.000), and intracellular ROS content (P=0.005). The expression levels of pro-apoptotic proteins (PARP, Bax and cleaved-caspase3) and p27Kip1 protein were downregulated, and the expression levels of Bcl-2, phospho-extracellular regulated protein kinases (P-ERK), phospho-protein kinase B (P-AKT), CDK2 etc. increased. Conclusion·The PDSORBS2 may inhibit H/R-induced apoptosis of H9C2 cells through the ERK/AKT/CDK2/p27Kip1 signaling pathway. [ABSTRACT FROM AUTHOR]

Gadd45 protein is a stress protein that responds to the environment and plays an important role in the regulation of various cell functions such as DNA repair, cell cycle and senescence and genotoxic stress. These proteins include three subtypes: α, β and γ. A large number of studies have shown that they are involved in the regulation of various signaling pathways in tumor cells, which are closely related to the occurrence and development of tumors, and their expression are closely related to tumor prognosis. In this paper, we briefly introduce and elaborate the research progress of Gadd45 protein family in tumor development in recent years.

Lung cancer is the leading cause of cancer deaths throughout the world. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. In traditional anti-cancer therapy, promotion of apoptosis in NSCLC is an important part of treatment, but anticancer drugs have the toxic side effects, resistance and other problems. Therefore, the search for new targets of anticancer drugs becomes one of the foci in the treatment of NSCLC. The BH3-only protein plays an important role in activation and communication in apoptosis pathways. BIM is the core member in BH3-only protein family. The target at BIM in the treatment of NSCLC has an irreplaceable role. This paper briefly describes the BCL-2 family and BH3-only pro-apoptotic protein, elaborates the important role of BIM and BH3-only protein in targeted therapy of NSCLC.