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驱动蛋白家族成员 2C 通过激活 MEK/ERK 通路促进肝癌生长和转移。

Kinesin family member 2C promotes hepatocellular carcinoma growth and metastasis via activating MEK/ERK pathway.

机构信息

Department of Infectious Diseases, QingDao No. 6 People's Hospital, Qingdao, Shandong, P. R. China.

Department of Blood Purification Center, QingDao No. 6 People's Hospital, Qingdao, Shandong, P. R. China.

出版信息

Biosci Biotechnol Biochem. 2021 Oct 21;85(11):2241-2249. doi: 10.1093/bbb/zbab154.

Abstract

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.

摘要

本研究旨在探索驱动蛋白家族成员 2C(KIF2C)在肝细胞癌(HCC)中的功能和作用机制。研究发现,KIF2C 在 HCC 中呈高表达状态,且预示着不良预后。沉默 KIF2C 可显著抑制 HCC 细胞的增殖、迁移和侵袭。此外,沉默 KIF2C 可明显下调 HCC 细胞中 Snail、Vimentin、p-MEK 和 p-ERK 的表达,而上调 E-cadherin 的表达。此外,我们还发现 MEK/ERK 抑制剂 U0126 可增强沉默 KIF2C 对 HCC 细胞增殖、迁移和侵袭的影响。相反,MEK/ERK 激活剂 PAF 可削弱沉默 KIF2C 对 HCC 细胞的影响。综上,本研究结果表明 KIF2C 可通过激活 MEK/ERK 通路促进 HCC 的增殖、迁移和侵袭。

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