Department of Physical Therapy, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China.
Department of Liver Disease, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China.
Technol Cancer Res Treat. 2021 Jan-Dec;20:15330338211007253. doi: 10.1177/15330338211007253.
This study aimed to evaluate the effects of centromere protein W (CENPW, also known as CUG2) in hepatocellular carcinoma (HCC).
CENPW expression in HCC tissues and cells was detected by RT-qPCR assay. CCK-8 and colony formation assay were used to assess cell proliferation. Wound healing and Transwell assay was used to detect cell migration and invasion, respectively. The flow cytometry was used to analyze the cell cycle distribution and apoptosis.
CENPW expression was upregulated in HCC tissues and cells. Knockdown of CENPW inhibited cell proliferation, migration, and invasion and induced the G0/G1 phase arrest and cell apoptosis in HCC cells, which might involve the E2F signaling regulation.
CENPW acted as an oncogenic role in HCC progression via activation E2F signaling. Our findings may provide new insights into the studying mechanisms of HCC.
本研究旨在评估着丝粒蛋白 W（CENPW，也称为 CUG2）在肝细胞癌（HCC）中的作用。
通过 RT-qPCR 检测 HCC 组织和细胞中的 CENPW 表达。使用 CCK-8 和集落形成实验评估细胞增殖。划痕愈合和 Transwell 实验分别用于检测细胞迁移和侵袭。流式细胞术用于分析细胞周期分布和细胞凋亡。
CENPW 在 HCC 组织和细胞中表达上调。敲低 CENPW 抑制 HCC 细胞的增殖、迁移和侵袭，并诱导 G0/G1 期阻滞和细胞凋亡，这可能涉及 E2F 信号调节。
CENPW 通过激活 E2F 信号在 HCC 进展中发挥致癌作用。我们的研究结果可能为 HCC 的研究机制提供新的见解。
