Vigilin is overexpressed in hepatocellular carcinoma and is required for HCC cell proliferation and tumor growth

Yang,Wen Li; Wei,Ling; Huang,Wen Qing; Li,Ran; Shen,Wen Yan; Liu,Jian Yu; Xu,Jian Ming; Li,Bo; Qin,Yang

doi:10.3892/or.2014.3111

Vigilin is overexpressed in hepatocellular carcinoma and is required for HCC cell proliferation and tumor growth

Authors:
- Wen Li Yang
- Ling Wei
- Wen Qing Huang
- Ran Li
- Wen Yan Shen
- Jian Yu Liu
- Jian Ming Xu
- Bo Li
- Yang Qin
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Affiliations: Department of Biochemistry and Molecular Biology, School of Preclinical and Forensic Medicine, West China Medical Center, Sichuan University, Chengdu, Sichuan 610041, P.R. China, Institute for Cancer Medicine, Luzhou Medical College, Luzhou, Sichuan 646000, P.R. China, Department of General Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China
Published online on: March 24, 2014 https://doi.org/10.3892/or.2014.3111
Pages: 2328-2334

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Abstract

Vigilin contains multiple KH domains and is an evolutionarily conserved RNA-binding protein from yeast to the human. Its reported roles in human carcinogenesis are controversial in different types of human cancers. To obtain the specific expression profiles of vigilin in human hepatocellular carcinomas (HCCs), we examined vigilin protein levels in normal human liver, liver cirrhosis, adjacent non-tumor liver and HCC tumor tissues as well as in several HCC cell lines. We discovered that vigilin expression increased progressively from the liver cirrhosis tissue to adjacent non-tumor liver tissue and then to HCC tumor cells. Vigilin protein was also overexpressed in all three HCC cell lines examined, HepG2, BEL7402 and SMMC7721, when compared with the vigilin expression level in the L-02 human embryonic hepatocyte cell line. We further investigated the impact of vigilin knockdown on HCC cell proliferation, survival, motility, tumor growth and sensitivity to chemotherapy. We found that knockdown of vigilin in the BEL7402 HCC cells significantly inhibited their proliferation, colony formation and migration, but largely enhanced the cisplatin treatment-induced growth inhibition of these cells in culture. We also found that vigilin knockdown effectively inhibited the growth of BEL7402 cell-derived xenograft tumors in nude mice by decreasing the proliferation and increasing the apoptosis of the BEL7402 HCC cells. Taken together, these results suggest that progressively upregulated vigilin may serve as a molecular risk marker for HCC development, and targeting vigilin may help to inhibit HCC cell growth, survival and migration.

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