Genomic instability is a hallmark of all cancers. RMI2 is a crucial component of the BLM-TopoIIIa-RMI1-RMI2 complex that maintains genome stability. It has been shown to accelerate tumor progression in lung cancer, cervical cancer, and prostate cancer. However, its expression and function in hepatocellular carcinoma (HCC) remain poorly defined. In this study, gene expression data and corresponding clinical information of HCC were downloaded from the TCGA, ICGC, and GEO databases. The expression level and clinical significance of RMI2 in HCC were then analyzed. In addition, cellular and molecular biology experiments were conducted to explore the effects of silencing and overexpression of RMI2 on human liver cancer cells and the associated mechanisms. The results showed that RMI2 expression was elevated in HCC tissues. High expression of RMI2 was correlated with shorter survival and poor prognosis of patients. The results of CCK-8, Edu, and clonogenic assays confirmed that RMI2 overexpression promoted the proliferation of HCC cells. Flow cytometric analysis demonstrated that RMI2 overexpression enhanced G1-S phase transition and decreased apoptosis. Moreover, the protein expression of key effector molecules in the p53 signaling pathway was reduced following RMI2 overexpression. In summary, these results indicate that RMI2 promotes the growth of HCC cells and suppresses their apoptosis by inhibiting the p53 signaling pathway. This study provides new insights into the mechanisms driving HCC tumorigenesis and new therapeutic targets.
Keywords: Growth; Hepatocellular carcinoma; Prognosis; RMI2; p53.
© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.