Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This research aimed to explore the molecular mechanism of microRNA (miR)-106b in cell apoptosis of atherosclerosis (AS). Human aortic endothelial cells (HAECs) were divided into control group, oxidized-low-density lipoproteins (ox-LDL) group, miR-106b NC+ox-LDL group, miR-106b mimics+ox-LDL group, miR-106b mimics+PTEN+ox-LDL group, and miR-106b mimics+empty+ox-LDL group. Real-time fluorescence quantitative polymerase chain reaction, cholecystokinin, TdT-mediated biotinylated nick end-labeling assay, luciferase reporter gene assay, and flow cytometry analysis were performed to determine the morphology, proliferation, and apoptosis in HSECs. Moreover, the levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), Bcl-2, p-P13K, and p-AKT in HAECs were detected by western blot. MiR-106b was down-regulated in ox-LDL-induced HAECs. PTEN was the target gene of miR-106b-5p. Overexpression of PTEN inhibited the anti-apoptotic effect of miR-106b. Compared with the control group, the proportion and number of HAECs apoptosis and Bax, caspase-3, and caspase-9 expression in ox-LDL and miR-106b mimics+PTEN+ox-LDL groups were significantly increased (all P<0.05). Moreover, the activity of HAECs and Bcl-2 were decreased significantly (all P<0.05). Overexpression of miR-106b in ox-LDL-induced AS inhibited endothelial cell apoptosis. Furthermore, miR-106b might activate the PI3K/AKT pathway by down-regulating the expression of PTEN in ox-LDL-induced HAECs.
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PMID:Up-regulated miR-106b inhibits ox-LDL-induced endothelial cell apoptosis in atherosclerosis. 3213 Feb 90

Endometrial carcinoma is a type of gynecological cancer that originates in the endometrial epithelial tissue. Due to its high proliferation and ability to invade muscle tissue, it is one of the most common malignant tumors in the female reproductive system. Fatostatin is a small molecule non-sterol diarylthiazole derivative that acts as a chemical inhibitor of the sterol regulatory-element binding protein (SREBP) pathway. Previous studies have shown that fatostatin has an anti-tumor effect in some cancers. In this study, we investigated the effect of fatostatin on the growth, proliferation, apoptosis, migration and cell cycle of human endometrial carcinoma cells (HEC-1A and AN3 CA cells) using cholecystokinin (CCK) -8 method, clonogenicity assay, wound closure assay, Transwell migration assay and flow cytometer. We also examined its effect on the expression of apoptosis-associated protein (Caspase-3, Caspase-8 and Caspase-9) and level of lipid metabolism-related proteins, free fatty acid, and total cholesterol in cells. The growth of endometrial carcinoma xenografts was measured to confirm the effect of fatostatin in vivo. Our results showed that fatostatin inhibited the growth and proliferation of human endometrial carcinoma cells, changed their cell cycle and induced apoptosis. Based on the preliminary animal experiments, fatostatin also exhibited antitumor activity. The present study adds a new dimension to our understanding of the antitumor effects of fatostatin and provides an experimental basis for its use, and supports its potential value for clinical application.
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PMID:Fatostatin inhibits the development of endometrial carcinoma in endometrial carcinoma cells and a xenograft model by targeting lipid metabolism. 3214 90


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