BACKGROUND: MicroRNAs (miRNA) are a group of noncoding small RNAs that repress mRNA expression or induce mRNA degradation by binding to the 3'-untranslated regions of mRNAs. MiRNAs have been connected closely with the development of cancers such as hepatocellular carcinoma (HCC). However, the overexpression of microRNA-301a (miR-301a) has seldom been connected with tumorigenesis in HCC. AIMS: This study aims to characterize the function of upregulated miR-301a in HCC and show how the downstream growth arrest-specific homeobox (Gax) is negatively regulated by miR-301a. METHODS: The expression of miR-301a and Gax was detected using real-time PCR on HCC tissues and adjacent non-tumorous tissues. The luciferase reporter assay was used to assess Gax as a target of miR-301a. The nuclear factor κB (NF-κB) was measured by western blot after inhibiting miR-301a and enhancing Gax. The functions of miR-301a in vivo in HCC cells were measured by migration and invasion assays and flow cytometry. RESULTS: MiR-301a was significantly upregulated and Gax was downregulated in HCC samples compared with in the matching nontumoral tissues. Inhibiting miR-301a expression caused the upregulation of Gax and repressed NF-κB expression. We have shown that miR-301a plays an important role in increasing proliferation, migration and invasion and in inhibiting apoptosis of HCC cells. CONCLUSIONS: miR-301a is frequently upregulated in HCC and modulates NF-κB expression by negatively regulating Gax.
BACKGROUND: MicroRNAs (miRNA) are a group of noncoding small RNAs that repress mRNA expression or induce mRNA degradation by binding to the 3'-untranslated regions of mRNAs. MiRNAs have been connected closely with the development of cancers such as hepatocellular carcinoma (HCC). However, the overexpression of microRNA-301a (miR-301a) has seldom been connected with tumorigenesis in HCC. AIMS: This study aims to characterize the function of upregulated miR-301a in HCC and show how the downstream growth arrest-specific homeobox (Gax) is negatively regulated by miR-301a. METHODS: The expression of miR-301a and Gax was detected using real-time PCR on HCC tissues and adjacent non-tumorous tissues. The luciferase reporter assay was used to assess Gax as a target of miR-301a. The nuclear factor κB (NF-κB) was measured by western blot after inhibiting miR-301a and enhancing Gax. The functions of miR-301a in vivo in HCC cells were measured by migration and invasion assays and flow cytometry. RESULTS:MiR-301a was significantly upregulated and Gax was downregulated in HCC samples compared with in the matching nontumoral tissues. Inhibiting miR-301a expression caused the upregulation of Gax and repressed NF-κB expression. We have shown that miR-301a plays an important role in increasing proliferation, migration and invasion and in inhibiting apoptosis of HCC cells. CONCLUSIONS:miR-301a is frequently upregulated in HCC and modulates NF-κB expression by negatively regulating Gax.
Authors: R C Smith; D Branellec; D H Gorski; K Guo; H Perlman; J F Dedieu; C Pastore; A Mahfoudi; P Denèfle; J M Isner; K Walsh Journal: Genes Dev Date: 1997-07-01 Impact factor: 11.361
Authors: Yun Chen; Malathi Banda; Cecilia L Speyer; Jennifer S Smith; Arnold B Rabson; David H Gorski Journal: Mol Cell Biol Date: 2010-06-01 Impact factor: 4.272
Authors: Elisa Frullanti; Antonella Galvan; Felicia S Falvella; Giacomo Manenti; Francesca Colombo; Alberto Vannelli; Matteo Incarbone; Marco Alloisio; Mario Nosotti; Luigi Santambrogio; Anna Gonzalez-Neira; Ugo Pastorino; Tommaso A Dragani Journal: Clin Cancer Res Date: 2011-01-17 Impact factor: 12.531
Authors: S A Ciafrè; S Galardi; A Mangiola; M Ferracin; C-G Liu; G Sabatino; M Negrini; G Maira; C M Croce; M G Farace Journal: Biochem Biophys Res Commun Date: 2005-09-09 Impact factor: 3.575
Authors: Jinmai Jiang; Yuriy Gusev; Ileana Aderca; Teresa A Mettler; David M Nagorney; Daniel J Brackett; Lewis R Roberts; Thomas D Schmittgen Journal: Clin Cancer Res Date: 2008-01-15 Impact factor: 12.531
Authors: Iván Lyra-González; Laura E Flores-Fong; Ignacio González-García; David Medina-Preciado; Juan Armendáriz-Borunda Journal: World J Hepatol Date: 2015-06-18