FEN1 Promotes Hepatocellular Carcinoma Progression by Activating Cell Cycle Transition from G2 To M Phase

被引:3
|
作者
Wang, Rangrang [1 ]
Zhang, Haijiao [1 ]
Huang, Dan [3 ]
Xu, Junming [2 ]
Zhang, Yang [1 ,4 ]
Wang, Tao [2 ,5 ]
机构
[1] Fudan Univ, Huadong Hosp, 221 West Yanan Rd, Shanghai, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai Gen Hosp, Dept Gen Surg, Shanghai, Peoples R China
[3] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 6, Sch Med, Digest Endoscop Ctr, Shanghai, Peoples R China
[4] Fudan Univ, Huadong Hosp, 221 West Yanan Rd, Shanghai 200040, Peoples R China
[5] Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Gen Surg, 85 Wujin Rd, Shanghai 200080, Peoples R China
来源
JOURNAL OF CANCER | 2024年 / 15卷 / 04期
基金
中国国家自然科学基金;
关键词
Flap endonuclease 1; Hepatocellular carcinoma; Cell cycle; G2/M transition; CANCER; ENDONUCLEASE; GENE;
D O I
10.7150/jca.88160
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Flap endonuclease 1 (FEN1) is a structure -specific nuclease that is involved in the occurrence and development of various types of tumors. Previous studies have shown that FEN1 plays an important role in the development of hepatocellular carcinoma, however, the molecular mechanisms remain fully elucidated, especially its effect on the cell cycle of hepatocellular carcinoma has not been investigated. In this study, via bioinformatics prediction and clinical specimen verification, we confirmed that FEN1 was highly expressed in HCC and correlated with poor prognosis. The knockdown or overexpression of FEN1 could inhibit or promote the proliferation and invasion of HCC cells. Importantly, cell cycle and functional experiments showed that FEN1 could promote cell proliferation by inducing cell cycle transition from G2 to M phase. Further studies indicated that FEN1 regulated the G2/M transition by modulating cell division cycle 25C (Cdc25C), cyclin-dependent kinase 1 (CDK1) and Cyclin B1 expressions. To sum up, our research suggested that FEN1 could promote the proliferation, migration and invasion of HCC cells via activating cell cycle progression from G2 to M phase, indicating that FEN1 may be a potential target for the treatment of HCC.
引用
收藏
页码:981 / 989
页数:9
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