JianDe Gong1, XuFei Qi1, Yi Zhang1, YingCong Yu2, XiZhou Lin2, HongLiang Li3, YiRen Hu4. 1. Department of Gastroenterology, Yinzhou People's Hospital, Ningbo, Zhejiang, China. 2. Department of Gastroenterology, Wenzhou No. 3 Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, Zhejiang, China. 3. Department of Gastroenterology, Yinzhou People's Hospital, Ningbo, Zhejiang, China. Electronic address: jiandegong@hotmail.com. 4. Medical College of Soochow University, Suzhou, Jiangsu, China; Department of General Surgery, Wenzhou No. 3 Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, Zhejiang, China. Electronic address: yirenhu@hotmail.com.
Abstract
BACKGROUND: Hepatocellular carcinoma (HCC) represents one of the most common malignancies worldwide. In two pubic long noncoding RNA (lncRNA) profiling studies of HCC, linc00462 was consistently upregulated. We analyzed the clinical significance and biological role of linc00462 in HCC. METHODS: We performed quantitative real-time PCR analysis to determine the levels of linc00462 in HCC tissues from 49 patients. Functional analysis was performed in cell lines and in an animal model to support clinical findings. RESULTS: Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway. CONCLUSIONS: linc00462 may be a potential therapeutic target in HCC.
BACKGROUND:Hepatocellular carcinoma (HCC) represents one of the most common malignancies worldwide. In two pubic long noncoding RNA (lncRNA) profiling studies of HCC, linc00462 was consistently upregulated. We analyzed the clinical significance and biological role of linc00462 in HCC. METHODS: We performed quantitative real-time PCR analysis to determine the levels of linc00462 in HCC tissues from 49 patients. Functional analysis was performed in cell lines and in an animal model to support clinical findings. RESULTS: Our data showed that linc00462 was significantly upregulated in HCC tissues compared with matched normal tissues. The knockdown of linc00462 in HCC cells resulted in a much less aggressive oncogenic phenotype, and linc00462 downregulation contribute to the inactivation of the PI3K/AKT signaling pathway. CONCLUSIONS:linc00462 may be a potential therapeutic target in HCC.