Background: Liver cancer (LIHC) is a malignant tumor that occurs in the liver and has a high mortality in cancer. The family genes were identified as tumor suppressor genes. Dysregulated expression of these genes can lead to cell cycle arrest, senescence and/or apoptosis. family genes are promising targets for anticancer therapy. However, their role in LIHC is still not well understood.
Aim: To have a better understanding of the important roles of family members in LIHC.
Methods: A series of bioinformatics approaches (including gene expression analysis, genetic alteration analysis, survival analysis, immune infiltration analysis, prediction of upstream microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) of , and -related gene functional enrichment analysis) was applied to study the expression profile, clinical relationship, prognostic significance and immune infiltration of in LIHC. The relationship between family genes expression and tumor associated immune checkpoints was investigated in LIHC. The molecular mechanism of mediated hepatocarcinogenesis was preliminarily discussed.
Results: mRNA/protein expression of different family genes in LIHC was analyzed in different databases, showing that family genes were highly expressed in LIHC. In 47 samples from 366 LIHC patients, the family genes were altered at a rate of 13%. By comprehensively analyzing the expression, clinical pathological parameters and prognostic value of family genes, was identified. was related to poor prognosis of LIHC, suggesting that they may play key roles in LIHC tumorigenesis and progression. One of the target miRNAs of was identified as hsa-miR-214-3p. Two upstream lncRNAs of hsa-miR-214-3p, U91328.1, and HCG17, were identified. At the same time, we found that the expression of family genes was correlated with immune cell infiltration and immune checkpoint genes.
Conclusion: This study lays a foundation for further research on the potential mechanism and clinical value of family genes in the treatment and prognosis of LIHC.
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| http://dx.doi.org/10.4251/wjgo.v16.i6.2592 | DOI Listing |
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