Propofol suppressed cell proliferation and enhanced apoptosis of bladder cancer cells by regulating the miR-340/CDK2 signal axis

xlomafota13 shared this article with you from Inoreader Propofol suppressed cell proliferation and enhanced apoptosis of bladder cancer cells by regulating the miR-340/CDK2 signal axis Via histochem Acta Histochem. 2021 May 25;123(5):151728. doi: 10.1016/j.acthis.2021.151728. Online ahead of print. ABSTRACT BACKGROUND: As widely reported, propofol can effectively inhibit tumors development. However, little is known about the molecular mechanisms. Here, we proved that propofol regulated miR-340/CDK2 axis to suppress bladder cancer progression in vitro. METHODS: MicroRNA (MiR)-340 expression in 5637 cells was examined using qRT-PCR. Cyclin-dependent kinase2 (CDK2) ex pression was detected using both qRT-PCR and western blot. The levels of apoptosis-related proteins and cell cycle-related proteins were evaluated using western blot. CCK-8 assay and BrdU assay were conducted to evaluate cell proliferation. Moreover, flow cytometry assay was employed to assess cell cycle and cell apoptosis. Finally, dual luciferase reporter assay was employed to verify the binding relationship between miR-340 and CDK2. RESULTS: Here we showed that propofol treatment inhibited cell proliferation of 5637 cells but enhanced cell apoptosis. Propofol upregulated miR-340 in a dose and time dependent manner. MiR-340 inhibitor could reverse the effect of propofol on the proliferation and apoptosis of 5637 cells. Next, dual luciferase reporter assay displayed that miR-340 directly bound to the 3'-UTR of CDK2. Finally, inhibition of CDK2 could partly reversed the effect of miR-340 inhibitor on cell proliferation and cell apoptosis of propofol-treated 5637 cells. C ONCLUSION: In total, our results proved that targeting miR340/CDK2 axis was novel to enhance the anti-tumor effects of propofol in bladder cancer in vitro, and our study provided alternative therapeutic strategies for clinical treatment of bladder cancer. PMID:34048990 | DOI:10.1016/j.acthis.2021.151728 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.