Z Zhao1, J Li, F Shen. 1. Medical College of Soochow University, Suzhou, China. shenfengsmmu@163.com.
Abstract
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.
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.