Propofol, an intravenous anaesthetic agent, has been found to exhibit antitumour effects in various kinds of cancer cells. However, the potential roles and regulatory mechanisms of propofol in oral squamous cell carcinoma (OSCC) remain unknown. Herein, we found that propofol inhibits OSCC cell growth and promotes cell apoptosis in a dose- and time-dependent manner. Further mechanistic studies revealed that the long noncoding RNA GAS5 is induced by propofol in OSCC cells. Elevated GAS5 acts as a competing endogenous RNA for miR-1297 and attenuates its inhibitory effect on GSK3β, leading to GSK3β increase and Mcl1 decrease. Additionally, we found that FoxO1 binds to the promoter of GAS5, facilitating its transcription in response to propofol treatment. Thus, these results suggest that propofol exhibits antitumour effects in OSCC cells and that the FoxO1-GAS5-miR-1297-GSK3β axis plays an important role in propofol-induced OSCC cell apoptosis.

中文翻译：

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GAS5是FoxO1激活的长非编码RNA，它通过调节miR-1297-GSK3β轴来促进异丙酚诱导的口腔鳞状细胞癌的凋亡。

丙泊酚，一种静脉麻醉剂，已被发现在各种癌细胞中具有抗肿瘤作用。但是，异丙酚在口腔鳞状细胞癌（OSCC）中的潜在作用和调控机制仍然未知。在本文中，我们发现丙泊酚以剂量和时间依赖性方式抑制OSCC细胞生长并促进细胞凋亡。进一步的机理研究表明，异丙酚可在OSCC细胞中诱导长的非编码RNA GAS5。升高的GAS5充当miR-1297的竞争内源RNA，并减弱其对GSK3β的抑制作用，导致GSK3β升高和Mcl1降低。此外，我们发现FoxO1与GAS5的启动子结合，从而促进其对丙泊酚治疗的转录反应。从而，