P14.5 functions to inhibit cell migration and can be used as a prognostic marker in hepatocellular carcinoma

P14.5 具有抑制细胞迁移的作用,可作为肝细胞癌的预后标志物

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作者:Sa Song #, Jian Pan #, Yaoyao Zhang, Yuehuan Xu, Qingmei Zhang, Xiaoxun Xie, Qingniao Zhou, Farong Mo, Guorong Luo, Naixia Chao

Background

Hepatocellular carcinoma (HCC) is the most common primary liver malignancy with a high mortality rate. P14.5 is a member of the highly conserved YER057c/YIL051c/YjgF subfamily and is highly expressed in the liver. However, its low expression is associated with carcinogenesis in HCC.

Conclusions

P14.5 may serve as a prognostic biomarker in HCC and plays a role in the migration and proliferation of HCC cells. Low expression of P14.5 during hepatocarcinogenesis is not attributed to DNA methylation.

Methods

The clinical significance of P14.5 in HCC was examined using ONCOMINE, UALCAN, Human Protein Atlas, and Kaplan-Meier plotter. The DNA methylation profile of the P14.5 promoter was examined in 103 HCC and paired precancerous tissues; the HCC cell lines HepG2, MHCC-97L, SMMC-7721, SK-Hep-1, and Huh7; and the normal hepatic cell line HL-7702 via MALDI-TOF mass spectrometry. In addition, in vitro experiments were performed to examine the effects of P14.5 overexpression on the proliferation and migration of SMMC-7721 cells.

Objective

This study aimed to investigate the role and prognostic significance of P14.5 in HCC.

Results

Low expression of P14.5 was correlated with shorter overall survival (OS) and disease-free survival (DFS) in HCC. Based on the results of MALDI-TOF mass spectrometry, no difference was observed in the methylation level between HCC cells and normal human hepatic cells and between HCC and paired precancerous tissues. Additionally, P14.5 overexpression promoted the proliferation and inhibited the migration of SMMC7721 cells in vitro. Conclusions: P14.5 may serve as a prognostic biomarker in HCC and plays a role in the migration and proliferation of HCC cells. Low expression of P14.5 during hepatocarcinogenesis is not attributed to DNA methylation.

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