Immune-Related lncRNAs with WGCNA Identified the Function of SNHG10 in HBV-Related Hepatocellular Carcinoma.

OBJECTIVE

The hepatitis B virus (HBV) infection led to hepatitis, which was one of common reasons for hepatocellular carcinoma (HCC). The immune microenvironment alteration played a crucial role in this process. The study aimed to identify immune-related long noncoding RNAs (lncRNAs) in HBV-related HCC and explore potential mechanisms.

METHODS

In total, 1,072 immune-related genes (IRGs) were enriched in different co-expression modules with weighted gene co-expression network analysis (WGCNA) combining the corresponding clinical features in HBV-related HCC. The immune-related lncRNAs were selected from the crucial co-expression model based on the correlation analysis with IRGs. The immune-related lncRNAs were furtherly used to construct prognostic signature by the Cox proportional hazards regression and Lasso regression. Furthermore, the proliferation and migration ability of lncRNA SNHG10 were verified in vitro.

RESULTS

A total of nine co-expression modules were identified by WGCNA of which the "red" co-expression module was most correlated with various clinical characteristics. Additionally, the IRGs in this module were significantly enriched in multiple immune-related pathways. The twelve immune-related lncRNAs prognostic signature (HAND2-AS1, LINC00844, SNHG10, MALAT1, LINC00460, LBX2-AS1, MIR31HG, SEMA6A-AS1, LINC1278, LINC00514, CTBP-AS2, and LINC00205) was constructed. The risk score was an independent risk factor in HBV-related HCC and verified by principal components analysis (PCA), nomogram, and PCR between different cell lines. Moreover, the proportion of immune cells were significantly different between high-risk score group and low-risk score group. The malignant behavior of Hep3B was significantly different between si-lncRNA SNHG10 and control group.

CONCLUSIONS

The immune-related lncRNAs prognostic signature provided some potential biomarkers and molecular mechanisms in HBV-related HCC.