Protective effect of the RNA-binding protein RBM10 in hepatocellular carcinoma

Objective To illustrate the protective effect of RBM10 on hepatocellular carcinoma (HCC) progression and the molecular mechanism. Patients and methods RBM10 levels in HCC tissues classified by tumor size and tumor node metastasis (TNM) staging were detected by quantitative real-time polymerase chain reaction (qRT-PCR) Chi-square test was conducted to reveal the relationship between RBM10 level and pathological features in HCC patients. The prognostic potential of RBM10 in HCC was assessed via the Kaplan-Meier method. Overexpression of RBM10 was achieved by transfection of LV-RBM10 in HepG2 and HCC-LM3 cells. Cell counting kit-8 (CCK-8) assay and flow cytometry were carried out to detect viability and apoptosis in HCC cells, respectively. In addition, invasive ability was assessed by transwell assay. Protein level of cleaved-caspase-3 was examined by Western blot. Regulatory effects of RBM10 on protein levels of EGFR, ERK and p-ERK were determined. Results RBM10 was downregulated in HCC tissues. Its level was markedly lower in HCC cases with larger tumor size and stage III+IV. Low level of RBM10 predicted poor prognosis in HCC patients. Overexpression of RBM10 suppressed viability and invasiveness in HCC-LM3 and HepG2 cells, but enhanced apoptotic rate and protein level of cleaved-caspase-3. EGFR was upregulated in HCC tissues, which was negatively regulated by RBM10. Overexpression of RBM10 downregulated protein levels of EGFR and p-ERK in HCC-LM3 and HepG2 cells. Conclusions RBM10 is downregulated in HCC tissues, which is favorable to the prognosis in HCC patients. As a tumor suppressor, RBM10 attenuates proliferative and invasive abilities, but drives apoptosis in HCC cells, thus alleviating the progression of HCC.