CDCA2 通过 AKT-mTOR 通路促进 HCC 细胞的发展。
CDCA2 Promotes HCC Cells Development via AKT-mTOR Pathway.
机构信息
Department of Radiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, China.
Department of Interventional Radiology, Harbin Medical University Cancer Hospital, Harbin 150001, China.
出版信息
Anal Cell Pathol (Amst). 2022 Dec 22;2022:9912254. doi: 10.1155/2022/9912254. eCollection 2022.
BACKGROUND
Hepatocellular carcinoma (HCC) is a highly aggressive and solid malignancy with a poor prognosis. Cell division cycle associated 2 (CDCA2) is highly expressed in HCC and is considered to be closely related to the prognosis of patients with HCC. In this research, we aimed to investigate the function and potential mechanism of CDCA2 in HCC cells.
METHODS
Gain- and loss-of-function experiments were conducted to determine the biological function of CDCA2 in HCC cells. Quantitative reverse transcription-polymerase chain reaction and western blot were utilized to examine the Messenger RNA (mRNA) and protein levels of CDCA2 in HCC cells. The malignant behaviors of HCC cells were analyzed by several biological experiments including cell viability, cell colony formation, and transwell assays. Western blot was also implemented to examine the expression of : AKT, protein kinase B and mTOR, mammalian target of rapamycin (AKT-mTOR) pathway related proteins and Cyclin D1.
RESULTS
A significant increase of CDCA2 was observed in HCC cell lines. Upregulation of CDCA2 resulted in the enhancement of the growth, migration, and invasion of HCC cells. Inversely, depletion of CDCA2 displayed the opposite results. Furthermore, the protein levels of p-AKT, p-mTOR, and Cyclin D1 were elevated with CDCA2 upregulation and reduced with CDCA2 depletion in HCC cells.
CONCLUSION
Our observations revealed that CDCA2 promoted the malignant development of HCC cells, and AKT-mTOR pathway might involve in the underlying mechanism.
背景
肝细胞癌（HCC）是一种高度侵袭性和实体恶性肿瘤，预后不良。细胞分裂周期相关蛋白 2（CDCA2）在 HCC 中高度表达，被认为与 HCC 患者的预后密切相关。在这项研究中，我们旨在研究 CDCA2 在 HCC 细胞中的功能和潜在机制。
方法
通过增益和缺失功能实验来确定 CDCA2 在 HCC 细胞中的生物学功能。定量逆转录-聚合酶链反应和 Western blot 用于检测 HCC 细胞中 CDCA2 的信使 RNA（mRNA）和蛋白水平。通过细胞活力、细胞集落形成和 Transwell 分析等多种生物学实验分析 HCC 细胞的恶性行为。Western blot 还用于检测 AKT、蛋白激酶 B 和哺乳动物雷帕霉素靶蛋白（AKT-mTOR）通路相关蛋白和细胞周期蛋白 D1 的表达。
结果
在 HCC 细胞系中观察到 CDCA2 的显著增加。CDCA2 的上调导致 HCC 细胞的生长、迁移和侵袭增强。相反，CDCA2 的耗竭则显示出相反的结果。此外，CDCA2 上调导致 HCC 细胞中 p-AKT、p-mTOR 和 Cyclin D1 的蛋白水平升高，而 CDCA2 耗竭则降低。
结论
我们的观察结果表明，CDCA2 促进了 HCC 细胞的恶性发展，AKT-mTOR 通路可能参与了潜在的机制。
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