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MiR-142-5p Suppresses Hepatocellular Carcinoma Cell Growth By Targeting IGF2BP3

Posted on:2017-05-04Degree:MasterType:Thesis
Country:ChinaCandidate:Y HuFull Text:PDF
GTID:2284330488467605Subject:Immunology
Abstract/Summary:PDF Full Text Request
Hepatocellular carcinoma (HCC) is a one of common malignancies and now the second leading cause of cancer death. HBV/HCV infection contributes to HCC development through different mechanisms, and both morbidity and mortality are high in our country. HCC tumorigenesis is relatively silent, and patients experience late symptomatic presentation. The option for curative treatments is limited to early stage of HCC, thus diagnosis and treatment in non-symptomatic individuals are crucial. MicroRNAs (miRNAs) are a large family of post-transcriptional regulators of gene expression that are approximately 21-25 nucleotides in length and control the developmental and cellular processes in most eukaryotic organisms. The contribution of miRNAs to cancer pathogenesis is well accepted as they can function as either oncogenes or tumor suppressor genes. In addition, potential value of miRNAs in clinical management of the patients with HCC has been demonstrated as some miRNAs may be used as prognostic, diagnostic markers or treatment strategy. Thus, microRNAs are a relatively new and efficient approach for potential early diagnosis cure for HCC. In our previous study, miRNAnome analysis of healthy liver tissues and HCC tissues suggested that miR-142-5p was downregulated in HCC tissue. In this study, we confirmed decreased expression of miR-142-5p in 88 HCC tissues compared with matched adjacent non-tumor tissues by q-PCR analysis. We found miR-142-5p could suppress cell growth of HCC in vitro and inhibit the G1/S transmission. Also miR-142-5p promoted the induction of apoptosis of HCC cells after treatment with doxorubicin. To explore the mechanism, we analysed the possible targets of miR-142-5p, and found miR-142-5p could directly target IGF2BP3, which involves in regulating apoptosis signaling pathway. Our experiments proved this presumption and showed over-expression of miR-142-5p promoted cell apoptosis by targeting IGF2BP3 and increasing caspase-3 expression in HCC cells. These findings suggest miR-142-5p could be a potential therapeutic target for the treatment of HCC.
Keywords/Search Tags:HCC, miR142-5p, proliferation, doxorubicin, apoptosis, IGF2BP3
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