This article aims to explore the effects and possible mechanism of miR-543 on small-cell lung carcinoma (SCLC) cells. The respective levels of miR-543 in lung carcinoma tissues, para-cancerous tissues, human normal lung cells MRC-9, and SCLC cells were detected by RT-qPCR. The proliferation, apoptosis, and migration of SCLC cells were detected after the miR-543 level in SCLC cells was altered by miRNA mimics and inhibitors. The levels of apoptosis-related proteins and potential downstream targeted proteins of miR-543 were detected by western blots. The study revealed that KNTC1 was highly expressed in lung carcinoma tissues and SCLC cells (P < 0.01). It also showed that knockdown of miR-543 can inhibit the proliferation and migration of SCLC cells, induce apoptosis, and increase the level of apoptosis-related proteins. These changes were reversed by the addition of mimics that increased miR-543 levels. The level of miR-543 was positively correlated with the protein expression level of downstream MUC1, β-catenin, and CDC42 in SCLC cells, suggesting that miR-543 may play a role through them. Thus this study concludes that MiR-543 can affect the function of SCLC cells, which may play a crucial role in the presence and development of SCLC.

中文翻译：

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敲低 miR-543 抑制小细胞肺癌细胞的增殖和迁移并诱导细胞凋亡。

本文旨在探讨miR-543对小细胞肺癌（SCLC）细胞的作用及其可能机制。RT-qPCR分别检测肺癌组织、癌旁组织、人正常肺细胞MRC-9和SCLC细胞中miR-543的水平。通过 miRNA 模拟物和抑制剂改变 SCLC 细胞中的 miR-543 水平后，检测到 SCLC 细胞的增殖、凋亡和迁移。通过蛋白质印迹检测miR-543的凋亡相关蛋白和潜在下游靶向蛋白的水平。研究表明，KNTC1在肺癌组织和SCLC细胞中高表达（P < 0.01）。还表明敲低 miR-543 可以抑制 SCLC 细胞的增殖和迁移，诱导细胞凋亡，增加凋亡相关蛋白的水平。通过添加增加 miR-543 水平的模拟物来逆转这些变化。miR-543的水平与SCLC细胞中下游MUC1、β-catenin和CDC42的蛋白表达水平呈正相关，提示miR-543可能通过它们发挥作用。因此本研究得出结论，MiR-543 可以影响 SCLC 细胞的功能，这可能在 SCLC 的存在和发展中起关键作用。