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Low expression of VSIG4 is associated with poor prognosis in hepatocellular carcinoma patients with hepatitis B infection

Authors Zhu S, Tan W, Li W, Zhou R, Wu X, Chen X, Li W, Shang C, Chen Y

Received 17 February 2018

Accepted for publication 28 May 2018

Published 20 September 2018 Volume 2018:10 Pages 3697—3705


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Harikrishna Nakshatri

Sicong Zhu,1,2,* Wenliang Tan,1,2,* Wenxin Li,1,2 Rui Zhou,1,2 Xiaolin Wu,1,2 Xianqing Chen,1,2 Wenda Li,2 Changzhen Shang,2 Yajin Chen2

1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China; 2Department of Hepatobiliary Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, People’s Republic of China

*These authors contributed equally to this work

Background: V-set and immunoglobulin domain containing protein 4 (VSIG4) was reported to play an important role in tumorigenesis. However, the expression and clinical relevance in hepatocellular carcinoma (HCC) remain unknown.
Materials and methods: First, the mRNA profiles of HCC were screened from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. VSIG4, a differentially expressed gene that has not been reported in HCC, was distinguished. Second, the correlation between VSIG4 expression and the prognosis of HCC patients from TCGA was analyzed. Third, VSIG4 mRNA level was detected in 36 pairs of HCC tissues and 4 HCC cell lines by PCR assay. And finally, prognosis analysis was assessed for 36 HCC patients with different expression levels of VSIG4.
Results: Bioinformatics analysis showed that VSIG4 expression was downregulated in HCC tissues, and the expression level of VSIG4 was negatively correlated with serum alpha fetal protein (AFP) level and tumor distant metastasis. Survival analysis of all HCC patients in TCGA indicated that the overall survival and disease-free survival were not significantly associated with VSIG4 expression. However, subgroup analysis showed that in the patients with hepatitis B virus-related HCC, both overall survival and disease-free survival were shorter in the low VSIG4 expression group. Our PCR results further showed that VSIG4 expression was significantly decreased in HCC tissues and HCC cell lines, and the disease-free survival in hepatitis B virus-related HCC patients with low VSIG4 expression was shorter than in those with high VSIG4 expression, which was consistent with the bioinformatics analysis results.
Conclusion: Our study suggests that VSIG4 is downregulated in HCC, and low expression of VSIG4 is associated with poor prognosis in hepatitis B virus-related HCC patients.

Keywords: hepatocellular carcinoma, VSIG4, hepatitis B infection, bioinformatics analysis

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