Abstract
Suppressor of cytokine signaling 3 (SOCS3) plays crucial roles in JAK/STAT signaling pathway inhibition in hepatocellular carcinoma (HCC). However, the methylation status of SOCS3 in HBV infection-related HCC and the relationship between SOCS3 methylation and the clinical outcome remain unknown. Here, we reported that in HCC tumor tissues, two regions of the CpG island (CGI) in the SOCS3 promoter were subjected to methylation analysis and only the region close to the translational start site of SOCS3 was hypermethylated. In HCC tumor tissues, SOCS3 showed an increased methylation frequency and intensity compared with that in the adjacent non-tumor tissues. Moreover, SOCS3 expression was significantly down-regulated in HCC cell lines and tumor tissues, and this was inversely correlated with methylation. Kaplan–Meier curve analysis revealed that in patients with an hepatitis B virus (HBV) infection background, SOCS3 hypermethylation was significantly correlated with a poor clinical outcome of HCC patients. Our findings indicated that SOCS3 hypermethylation has already happened in non-tumor tissues and increased in both frequency and intensity in tumor tissues. This suggests that the methylation of SOCS3 could predict a poor prognosis in HBV infection-related HCC patients.
Highlights
Hepatocellular carcinoma (HCC) is a common malignancy worldwide with rapid progress and high short-term mortality
We evaluated the prognostic value of the Suppressor of cytokine signaling 3 (SOCS3) methylation status in HCC patients
SOCS3 hypermethylation was significantly correlated with the poor prognosis of HCC patients with
Summary
Hepatocellular carcinoma (HCC) is a common malignancy worldwide with rapid progress and high short-term mortality. Mounting studies have revealed that HCC tumors exhibit specific DNA methylation signatures that are associated with major risk factors and tumor progression [8]. The methylation status of TSGs in HCC with different virus infection, especially HBV infection, is not fully understood. In our previous report, we did not observe SOCS3 hypermethylation in HBV-related HCC tissues [21]. These conflicting results may be due to the complicated etiological mechanism of HCC and the different detected loci in the SOCS3 promoter region. It is imperative to explore the detailed methylation status of SOCS3 in HCC with different virus infection backgrounds and the relationship between its methylation and clinicopathology. The clinicopathological significance of SOCS3 methylation status was statistically analyzed
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