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.

中文翻译：

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丙泊酚通过 miR-34a 介导的 E-钙粘蛋白和 LOC285194 信号抑制胰腺癌 PANC-1 细胞的迁移并诱导细胞凋亡。


异丙酚在体外和体内对胰腺癌细胞表现出有效的抗肿瘤活性。本研究旨在探讨异丙酚对胰腺癌PANC-1细胞的体外抗肿瘤机制。 PANC-1细胞暴露于浓度20μg/ml的异丙酚72小时。采用长非编码RNA LOC285194 siRNA LOC285194 siRNA、E-cadherin siRNA和microRNA-34a（miR-34a）抑制剂研究异丙酚对PANC-1细胞的影响。通过定量实时 PCR (qRT-PCR) 分析 miR-34a 和 LOC285194。通过Western blot分析促凋亡蛋白bax、cleaved-caspase-3和抗凋亡蛋白bcl-2。分别通过MTT和TUNEL染色检测细胞活力和细胞凋亡。通过伤口愈合测定检测细胞迁移。结果表明，丙泊酚上调miR-34a表达，进而上调LOC285194表达，导致PANC-1细胞凋亡和生长抑制。此外，丙泊酚上调 miR-34a 表达，进而上调 E-钙粘蛋白表达，导致细胞迁移抑制。我们的研究证实，异丙酚分别通过促进 miR-34a 依赖性 LOC285194 和 E-cadherin 上调来诱导 PANC-1 细胞凋亡并抑制细胞迁移。