Abstract

Abstract Hepatocellular carcinoma (HCC) is one of the most common and aggressive human malignancies worldwide. Most patients with HCC have an established background of chronic liver disease and cirrhosis, with major etiological and risk factors including chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV). Long non-coding (lnc)RNAs are a class of non-protein coding transcripts longer than 200 nucleotides that regulate complex cellular functions, such as cell growth, differentiation, metabolism and metastasis. Increasing evidence has shown that lncRNAs regulate gene expression by targeting the production, splicing, decay, or translation of target mRNAs. Although deregulation of lncRNAs expression have been detected in HCC or many tumor types, there are still many novel lncRNAs have not been studied and the mechanisms underlying functional impairment and specific involvement of lncRNAs during hepato-carcinogenesis remain to be established. Here, we aimed to investigate the involvement of specific dys-regulated lncRNA-FAM and its molecular mechanism. FAM is overexpressing in HCC and correlates with tumor size, vascular invasion, and pathology stage. Overexpression FAM accelerates cell proliferation, invasion in HCC cells. Further, FAM is induced in the Doxorubicin (DOX) resistance HCC cells show in the Gene Expression Omnibus (GEO) Datasets analysis. Overexpression FAM did increase DOX-resistant in two HCC cell lines. After overexpression FAM, lysosome-associated membrane protein 2 (LAMP2) expression was enhanced which also correlated with DOX-resistant. From the co-immunoprecipitation analysis, FAM directly interacted with LAMP2 to protect its ubiquitination. Thus, FAM may play an oncogenic role during hepato-carcinogenesis. Citation Format: Po-Shuan Huang, Kwang-Huei Lin. Overexpression of long noncoding RNA FAM promotes cancer invasion and drug resistance in human liver cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 847.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call