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Triptolide's impact on ACER1 signaling: Inducing autophagy for triple-negative breast cancer suppression.
Pathol Res Pract
January 2025
Clinical Pharmacy & Pharmacology Research Institute, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Affiliated Hospital of Guilin Medical University, Guilin 541001, China; Guangxi Health Commission Key Laboratory of Basic Research in Sphingolipid Metabolism Related Diseases, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China; China-USA Lipids in Health and Disease Research Center, Guilin Medical University,Guilin 541001, China; Laboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin 541001, China. Electronic address:
Given the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (Her-2) in triple-negative breast cancer (TNBC) cells, the efficacy of targeted therapies is limited. In this study, we uncovered that triptolide (TP) effectively suppresses the migration and invasiveness of MDA-MB-231 cells by activating autophagic pathways. Western blotting analysis revealed that TP significantly reduced the expression levels of p62 protein, while simultaneously markedly increasing the expression levels of LC3B-II, BNIP3, BNIP3L, ATG5, and ULK1 proteins, strongly suggesting an enhancement of autophagic activity in the cells.
View Article and Find Full Text PDFRespiratory complex I-mediated NAD regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21 expression by SIRT3 and SIRT7.
Mol Oncol
January 2025
Division of Cancer Cell Biology, Department of Pharmaceutical Sciences, Showa University Graduate School of Pharmacy, Tokyo, Japan.
The role of the electron transport chain (ETC) in cell proliferation control beyond its crucial function in supporting ATP generation has recently emerged. In this study, we found that, among the four ETC complexes, the complex I (CI)-mediated NAD regeneration is important for cancer cell proliferation. In cancer cells, a decrease in CI activity by RNA interference (RNAi) against NADH:ubiquinone oxidoreductase core subunit V1 (NDUFV1) arrested the cell cycle at the G/S phase, accompanying upregulation of p21 cyclin-dependent kinase inhibitor expression.
View Article and Find Full Text PDFHER2 regulates autophagy and promotes migration in gastric cancer cells through the cGAS-STING pathway.
Anticancer Drugs
January 2025
Department of General Surgery and Laboratory of Gastric Cancer, State Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy and Cancer Center.
In gastric cancer, the relationship between human epidermal growth factor receptor 2 (HER2), the cyclic GMP-AMP synthase-stimulator of the interferon genes (cGAS-STING) pathway, and autophagy remains unclear. This study examines whether HER2 regulates autophagy in gastric cancer cells via the cGAS-STING signaling pathway, influencing key processes such as cell proliferation and migration. Understanding this relationship could uncover new molecular targets for diagnosis and treatment.
View Article and Find Full Text PDFOptimizing Premenopausal Hormone Receptor-Positive Human Epidermal Growth Factor Receptor 2-Negative Early Breast Cancer Management in India: Insights From Expert Consensus.
Cureus
December 2024
Department of Medical Affairs, Dr. Reddy's Laboratories, Hyderabad, IND.
This research aims to optimize adjuvant ovarian function suppression (OFS) for premenopausal Indian women with hormone receptor-positive (HR+) /human epidermal growth factor receptor 2-negative (HER2-) early breast cancer (eBC). To address specific challenges identified in clinical practice, a comprehensive questionnaire consisting of 21 statements was developed. These statements were reviewed and validated by a scientific committee, ensuring their accuracy and relevance to the study's objectives.
View Article and Find Full Text PDFCombination of Carbonic Anhydrase Isoform IX Inhibitors and Gefitinib Suppresses on the Invasive Potential of Non-Small Cell Lung Cancer Cells.
Biochemistry (Mosc)
December 2024
Medicinal Chemistry Center, Togliatti State University, Togliatti, 445020, Russia.
Human carbonic anhydrase IX (CAIX) plays a key role in maintaining pH homeostasis of malignant neoplasms, thus creating a favorable microenvironment for the growth, invasion, and metastasis of tumor cells. Recent studies have established that inhibition of CAIX expressed on the surface of tumor cells significantly increases the efficacy of classical chemotherapeutic agents and makes it possible to suppress the resistance of tumor cells to chemotherapy, as well as to increase their sensitivity to drugs (in particular, to reduce the required dose of cytostatic agents). In this work, we studied the ability of new CAIX inhibitors based on substituted 1,2,4-oxadiazole-containing primary aromatic sulfonamides, to potentiate the cytostatic effect of gefitinib (selective inhibitor of epidermal growth factor receptor tyrosine kinase domain) under hypoxic conditions.
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