Propofol inhibits migration and induces apoptosis of pancreatic cancer PANC-1 cells through miR-34a-mediated E-cadherin and LOC285194 signals. Issue 1 (1st January 2020)

• Record Type: Journal Article
• Authors: Wang, Hongwei; Jiao, Hongmei; Jiang, Ziru; Chen, Renyi
• Is Part Of: Bioengineered. Volume 11:Issue 1(2020)
• Page Start: 510
• Page End: 521
• Publication Date: 2020-01-01
• Subjects: Pancreatic cancer -- microRNA-34a -- long non-coding RNA LOC285194 -- E-cadherin -- apoptosis -- migration; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2020.1754038
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: Propofol has exhibited potent antitumor activity in pancreatic cancer cells in vitro and in vivo . The study aimed to investigate the anti-tumor mechanisms of propofol on pancreatic cancer PANC-1 cells in vitro . PANC-1 cells were exposure to concentration 20 μg/ml of propofol for 72 h. Long non-coding RNA LOC285194 siRNA LOC285194 siRNA, E-cadherin siRNA and microRNA-34a (miR-34a) inhibitor were used to investigate the effect of propofol on PANC-1 cells. miR-34a and LOC285194 were analyzed by quantitative real-time PCR (qRT-PCR). Pro-apoptotic protein bax, cleaved-caspase-3 and anti-apoptotic protein bcl-2 were analyzed by Western blot. Cell viability and cell apoptosis were detected by MTT and TUNEL staining, respectively. Cell migration was detected by wound-healing assay. The results showed that propofol upregulated miR-34a expression, which, in turn, upregulated LOC285194 expression, resulting in PANC-1 cell apoptosis and growth inhibition. In addition, propofol upregulated miR-34a expression, which, in turn, upregulated E-cadherin expression, resulting in cell migration inhibition. Our research confirmed that propofol-induced cell apoptosis and inhibited cell migration in PANC-1 cells in vitro via promoting miR-34a-dependent LOC285194 and E-cadherin upregulation, respectively.