摘要
Hepatocellular carcinoma(HCC) is a leading cause of cancer mortality worldwide. Despite progress in the diagnosis and treatment of HCC, its prognosis still remains unfavorable. In accumulating studies, long non-coding RNAs(lncRNAs) are emerging as vital players in tumorigenesis and cancer progression. However, the molecular mechanisms and clinical significance of lncRNAs in HCC remain largely elusive. In this study, we analyzed lncRNA microarray expressionprofiles of tumor samples and its matched adjacent tissue samples from 10 HCC patients and found that the expression of RP11J20.1 in HCC tissues is makedly lower than adjacent tissues. Expression of RP11J20.1 was also remarkably downregulated in 112 HCC tissues and cell lines by qRT-PCR. Low RP11J20.1 expression was correlated with alphafetoprotein(AFP) level, tumor size and microvascular invasion. Kaplan-Meier survival analysis demonstrated that low RP11J20.1 expression predicts poor prognosis of HCC patients. Gain-of-function and loss-of-function experiments showed that RP11J20.1 promotes HCC cells proliferation, cell cycle progression, and inhibits HCC cells apoptosis. Further experiments revealed that RP11J20.1 promotes HCC cells proliferation through inhibiting STAT1 genes expression. Collectively, our results demonstrated the clinical prognostic significance and roles of RP11J20.1 in HCC, and suggested that RP11J20.1 may be considered as a prognostic biomarker and therapeutic target for HCC.
Hepatocellular carcinoma(HCC) is a leading cause of cancer mortality worldwide. Despite progress in the diagnosis and treatment of HCC, its prognosis still remains unfavorable. In accumulating studies, long non-coding RNAs(lncRNAs) are emerging as vital players in tumorigenesis and cancer progression. However, the molecular mechanisms and clinical significance of lncRNAs in HCC remain largely elusive. In this study, we analyzed lncRNA microarray expressionprofiles of tumor samples and its matched adjacent tissue samples from 10 HCC patients and found that the expression of RP11J20.1 in HCC tissues is makedly lower than adjacent tissues. Expression of RP11J20.1 was also remarkably downregulated in 112 HCC tissues and cell lines by qRT-PCR. Low RP11J20.1 expression was correlated with alphafetoprotein(AFP) level, tumor size and microvascular invasion. Kaplan-Meier survival analysis demonstrated that low RP11J20.1 expression predicts poor prognosis of HCC patients. Gain-of-function and loss-of-function experiments showed that RP11J20.1 promotes HCC cells proliferation, cell cycle progression, and inhibits HCC cells apoptosis. Further experiments revealed that RP11J20.1 promotes HCC cells proliferation through inhibiting STAT1 genes expression. Collectively, our results demonstrated the clinical prognostic significance and roles of RP11J20.1 in HCC, and suggested that RP11J20.1 may be considered as a prognostic biomarker and therapeutic target for HCC.
引文