FAM111B基因沉默通过激活p53信号通路抑制肝癌细胞的增殖、迁移和侵袭。

Silencing of FAM111B inhibited proliferation, migration and invasion of hepatoma cells through activating p53 pathway.

作者信息

Li Feng, He Hong-Ye, Fan Zhi-Hao, Li Chun-Ming, Gong Yi, Wang Xiao-Jun, Xiong Hao-Jun, Xie Chuan-Ming, Bie Ping

机构信息

Department of Hepatobiliary and Pancreatic Surgery, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, PR China.

Institute of Ultrasound Imaging & Department of Ultrasound, The Second Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ultrasound Molecular Imaging, Chongqing 400010, PR China.

出版信息

Dig Liver Dis. 2023 Dec;55(12):1679-1689. doi: 10.1016/j.dld.2023.05.002. Epub 2023 Jun 1.

DOI:10.1016/j.dld.2023.05.002

PMID:37270349

Abstract

BACKGROUND

The function of Family with sequence similarity 111 member B (FAM111B) has been reported in multiple malignancies, but its involvement in occurrence and development of hepatocellular carcinoma (HCC) is still unclear.

PURPOSE

To investigate the role of FAM111B in HCC and explore the potential molecular mechanism.

METHODS

We examined the mRNA level of FAM111B via qPCR and protein level via immunohistochemistry in human HCC tissues. siRNA was used to construct a FAM111B-knockdown model in HCC cell lines. CCK-8, colony formation, transwell, and wound healing assays were performed to investigate the effect of FAM111B on proliferation, migration and invasion of HCC cell. Gene Set Enrichment Analysis, western blotting, and flow cytometry were carried out to find the related molecular mechanism.

RESULTS

Human HCC tumor tissues exhibited higher expression of FAM111B, and high FAM111B expression was associated with poor prognosis. Vitro assays demonstrated that knockdown of FAM111B greatly repressed proliferation, migration and invasion of HCC cells. Furthermore, silencing of FAM111B significantly resulted in cell cycle arrest at G0/G1 and downregulation of epithelial-mesenchymal transition (EMT)-related proteins MMP7 and MMP9 via activation of p53 pathway.

CONCLUSION

FAM111B played an essential role in promoting HCC development by regulation of p53 pathway.

摘要

背景

序列相似性家族111成员B（FAM111B）在多种恶性肿瘤中的功能已有报道，但其在肝细胞癌（HCC）发生发展中的作用仍不清楚。

目的

研究FAM111B在HCC中的作用并探讨其潜在的分子机制。

方法

我们通过qPCR检测人HCC组织中FAM111B的mRNA水平，并通过免疫组织化学检测其蛋白水平。使用小干扰RNA（siRNA）在HCC细胞系中构建FAM111B敲低模型。进行CCK-8、集落形成、Transwell和伤口愈合试验，以研究FAM111B对HCC细胞增殖、迁移和侵袭的影响。进行基因集富集分析、蛋白质免疫印迹和流式细胞术以发现相关分子机制。