MiR-20a shows a significant role in the development of various human tumors. However, its specific biological function in non-small-cell lung cancer (NSCLC) is still not clear. qRT-PCR was applied for detecting miR-20a expression. The analysis of cell growth and apoptosis were performed by MTT, xenograft models, Western blot assays. Dual luciferase reporter, Western blotting and qRT-PCR were carried out to verify the potential target of miR-20a. In NSCLC tissues and cells, miR-20a was highly expressed and RUNX3 was lowly expressed. Moreover, up-regulation of miR-20a expression promoted NSCLC cell proliferation, invasion and migration, while low-expression of miR-20a showed the converse case on cell proliferation, invasion and migration. RUNX3 was verified as the direct target of miR-20a and it could overturn its biological function in NSCLC cells. Moreover, miR-20a negatively regulated RUNX3 expression. Mechanistically, increasing miR-20a expression inhibited RUNX3 expression and then activated the TGF-β signaling pathway. Taken together, our results demonstrated that re-expression of miR-20a promoted lung tumorigenesis by down-regulation of RUNX3 and facilitating the activation of TGF-β signaling pathway.
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http://dx.doi.org/10.23812/20-12A | DOI Listing |
Annu Rev Biomed Eng
January 2025
1Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana, USA; email:
Biochemical signals in native tissue microenvironments instruct cell behavior during many biological processes ranging from developmental morphogenesis and tissue regeneration to tumor metastasis and disease progression. The detection and characterization of these signals using spatial and highly resolved quantitative methods have revealed their existence as matricellular proteins in the matrisome, some of which are bound to the extracellular matrix while others are freely diffusing. Including these biochemical signals in engineered biomaterials can impart enhanced functionality and native-like complexity, ultimately benefiting efforts to understand, model, and treat various diseases.
View Article and Find Full Text PDFMol Pharm
January 2025
State Key Laboratory for Organic Electronics and Information Displays & Jiangsu Key Laboratory for Biosensors, Institute of Advanced Materials (IAM), Nanjing University of Posts & Telecommunications, Nanjing 210023, China.
Natural killer (NK) cell immunotherapy is a significant category in tumor therapy due to its potent tumor-killing and immunomodulatory effects. This research delves into exploring the mechanisms underlying the ability of amoxicillin to boost NK cell cytotoxicity in NK cell immunotherapy. Amoxicillin significantly enhances the cytotoxic activity of NK-92MI cells against MCF-7 cells by triggering the initiation of a cytolytic program in target cell-deficient NK-92MI cells and augmenting the degranulation level of NK-92MI cells in the presence of target cells.
View Article and Find Full Text PDFJ Med Chem
January 2025
Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, DK-2100 Copenhagen, Denmark.
The Ca/calmodulin-dependent protein kinase II α (CaMKIIα) plays a crucial role in regulating neuronal signaling and higher brain functions, being involved in various brain diseases. Utilization of small molecules targeting the CaMKIIα hub domain has proved to be a promising strategy for specific CaMKIIα modulation and future therapy. Through an structure-based virtual screening campaign, we herein identified 2-arylthiazole-4-carboxylic acids as a new class of high-affinity CaMKIIα hub ligands.
View Article and Find Full Text PDFShock
January 2025
Pharmacology, University of Vermont, Burlington, VT.
Objective: Loss of function of the phospholipid scramblase (PLS) TMEM16F results in Scott Syndrome, a hereditary bleeding disorder generally attributed to intrinsic platelet dysfunction. The role of TMEM16F in endothelial cells, however, is not well understood. We sought to test the hypothesis that endothelial TMEM16F contributes to hemostasis by measuring bleeding time and venous clotting in endothelial-specific knockout (ECKO) mice.
View Article and Find Full Text PDFJ Proteome Res
January 2025
Graduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Republic of Korea.
The E3 ubiquitin ligase neural precursor cell-expressed developmentally down-regulated 4 (NEDD4) is involved in various cancer signaling pathways, including PTEN/AKT. However, its role in promoting gastric cancer (GC) progression is unclear. This study was conducted to elucidate the role of NEDD4 in GC progression.
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