1. Long noncoding RNA linc00462 promotes hepatocellular carcinoma progression
- Author
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YingCong Yu, Xizhou Lin, Jian-De Gong, Hong-Liang Li, YiRen Hu, Xu-Fei Qi, and Yi Zhang
- Subjects
Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Carcinogenesis ,Down-Regulation ,Mice, Nude ,Mice ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Clinical significance ,neoplasms ,PI3K/AKT/mTOR pathway ,Pharmacology ,Gene knockdown ,Akt/PKB signaling pathway ,business.industry ,Liver Neoplasms ,General Medicine ,Middle Aged ,medicine.disease ,Phenotype ,digestive system diseases ,Long non-coding RNA ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Disease Progression ,Cancer research ,Female ,RNA, Long Noncoding ,business ,Signal Transduction - 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.
- Published
- 2017