To date, surgical resection is the mainstay for the treatment of colorectal cancer (CRC). Propofol (2,6-diisopropylphenol), one of the most commonly used intravenous anaesthetic agents, has been reported to be involved in modulating the malignancy of a variety of human cancers. However, the underlying mechanisms remain poorly understood. In this study, using a cell counting kit (CCK-8), flow cytometry, and caspase-3 cleavage assays, we found that propofol promoted cell apoptosis and inhibited cell proliferation in both Colo205 and SW620 cells, through the down-regulation of HOXA11-AS and up-regulation of let-7i. Moreover, gain-of-function studies of HOXA11-AS or loss-of-function studies of let-7i also revealed a negative correlation between HOXA11-AS and let-7i in propofol-mediated biological functions of CRC cells. Furthermore, our mechanistic experiments revealed that HOXA11-AS acts as a molecular sponge for let-7i, thereby regulating the expression of ABCC10. We investigate the theory that propofol suppresses colorectal cancer tumorigenesis by modulating the HOXA11-AS-let-7i-ABCC10 regulatory network, indicating the potential for propofol to control CRC development.

中文翻译：

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丙泊酚通过减轻对miRNA let-7i的lncRNA HOXA11-AS的抑制作用来促进大肠癌细胞的凋亡。

迄今为止，手术切除是治疗大肠癌（CRC）的主要手段。据报道，丙泊酚（2,6-二异丙基苯酚）是最常用的静脉麻醉药之一，其参与调节多种人类癌症的恶性程度。但是，基本机制仍然知之甚少。在这项研究中，我们使用细胞计数试剂盒（CCK-8），流式细胞仪和caspase-3裂解检测法，发现丙泊酚通过下调HOXA11的表达而促进Colo205和SW620细胞的细胞凋亡并抑制细胞增殖。 -AS和let-7i的上调。此外，HOXA11-AS的功能获得研究或let-7i的功能丧失研究也显示，HOXA11-AS和let-7i在丙泊酚介导的CRC细胞生物学功能中呈负相关。此外，我们的机械实验表明，HOXA11-AS充当let-7i的分子海绵，从而调节ABCC10的表达。我们研究了丙泊酚通过调节HOXA11-AS-let-7i-ABCC10调控网络来抑制大肠癌肿瘤发生的理论，表明丙泊酚可能控制CRC的发展。