FAXDC2 inhibits the proliferation and invasion of human liver cancer HepG2 cells

作者：Zhilin Peng, Siting Xu, Qing Zhang, Xueting Yang, Wuzhou Yuan, Yuequn Wang, Yongqing Li, Ping Zhu, Xiushan Wu, Zhigang Jiang, Fang Li, Xiongwei Fan · 发表于：Experimental and Therapeutic Medicine · 年份：2023 · DOI：10.3892/etm.2023.12315 · 被引用次数：6 · 研究领域：Cancer, Lipids, and Metabolism、Peroxisome Proliferator-Activated Receptors、Caveolin-1 and cellular processes

The reprogramming of lipid metabolism serves an important role in occurrence and development of liver cancer. Fatty acid hydroxylase domain containing 2 (FAXDC2) is a hydroxylase involved in the synthesis of cholesterol and sphingomyelin and downregulated in various types of cancer. There are no reports on the relationship between FAXDC2 and liver carcinogenesis. The present study used multiple portals and publicly available tools to explore its correlation with liver cancer. The results showed that the expression of FAXDC2 decreased in liver cancer and the methylation level near the promoter increased. Patients with liver cancer and with low expression of FAXDC2 had a poor prognosis. Gain of function and loss of function strategies were performed to evaluate its roles in liver cancer cells. CCK-8 assay showed that overexpression of FAXDC2 inhibited the viability of liver cancer cells (HepG2). Flow cytometry analysis indicated that HepG2 cells with overexpressing FAXDC2 showed an S phase arrest, associated with cyclin-dependent kinase 2 decreased. Transwell experiments showed that increasing FAXDC2 inhibited HepG2 cell invasion ability, accompanied by the upregulation of E-cadherin. Notably, knockdown of FAXDC2 had no significant effect on cell cycle and invasion functions. Based on the cBioPortal platform, FAXDC2 was predicted to closely correlate to the ERK signal in tumorigenesis. Western blotting results showed that overexpression of FAXDC2 decreased the phosphorylation l...