The current work was intended to explore the function and mechanism of Kinesin family member 2C (KIF2C) in hepatocellular carcinoma (HCC). In this study, KIF2C expression was at a high level in HCC and indicated poor prognosis. Silencing KIF2C significantly suppressed the proliferation, migration, and invasion in HCC cells. Furthermore, silencing KIF2C markedly decreased the expression of Snail, Vimentin, p-MEK, and p-ERK, but increased E-cadherin expression in HCC cells. Moreover, we also found that MEK/ERK inhibitor U0126 could enhance the impact on cell proliferation, migration, and invasion induced by silencing KIF2C in HCC. On the contrary, MEK/ERK activator PAF could weaken the impact induced by silencing KIF2C in HCC. Thus, our findings indicate that KIF2C can promote the proliferation, migration, and invasion by activating MEK/ERK pathway in HCC.

中文翻译：

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驱动蛋白家族成员 2C 通过激活 MEK/ERK 通路促进肝细胞癌的生长和转移。

目前的工作旨在探索驱动蛋白家族成员2C（KIF2C）在肝细胞癌（HCC）中的功能和机制。在这项研究中，KIF2C 在 HCC 中的表达水平很高，表明预后不良。沉默 KIF2C 显着抑制了 HCC 细胞的增殖、迁移和侵袭。此外，沉默 KIF2C 显着降低了 HCC 细胞中 Snail、Vimentin、p-MEK 和 p-ERK 的表达，但增加了 E-cadherin 的表达。此外，我们还发现 MEK/ERK 抑制剂 U0126 可以增强对 HCC 中 KIF2C 沉默诱导的细胞增殖、迁移和侵袭的影响。相反，MEK/ERK 激活剂 PAF 可以减弱 HCC 中由沉默 KIF2C 引起的影响。因此，我们的研究结果表明 KIF2C 可以促进增殖、迁移、