MicroRNA-4262 activates the NF-κB and enhances the proliferation of hepatocellular carcinoma cells
| Autor: | Guo-Yong Han, Yuan-Yuan Gao, Xin-Li Huang, Jindao Wu, Wenzhou Ding, Sen Lu |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Carcinoma Hepatocellular Apoptosis Biology Biochemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation Structural Biology microRNA Humans Luciferase Molecular Biology Cell Proliferation Cell growth Cell Cycle Liver Neoplasms Transcription Factor RelA RNA-Binding Proteins NF-κB Hep G2 Cells General Medicine Cell cycle digestive system diseases Up-Regulation MicroRNAs 030104 developmental biology chemistry 030220 oncology & carcinogenesis Cancer research Signal transduction Apoptosis Regulatory Proteins Signal Transduction |
| Zdroj: | International Journal of Biological Macromolecules. 86:43-49 |
| ISSN: | 0141-8130 |
| DOI: | 10.1016/j.ijbiomac.2016.01.019 |
| Popis: | microRNAs (miRNAs) were known as transcriptional regulators to regulate the repertoires of target genes during the development of hepatocellular carcinoma (HCC). In this study, we investigated the roles of miR-4262 in the process of HCC. Our results showed that miR-4262 is overexpressed in HCC tissues and hepatoma cell lines (HepG2 and Sk-hep-1). We also found that miR-4262 enhanced the process of cell cycle and inhibited the apoptosis leading to promoted cell proliferation and activity. Moreover, the 3'UTR of PDCD4 was complementary to miR-4262 seed region and we confirmed that PDCD4 is the direct target of miR-4262 with 3'UTR luciferase assay. qPCR and WB analysis revealed that the level of PDCD4 was negatively correlated with the expression of miR-4262 in HepG2 cells. Furthermore, our results demonstrated that miR-4262-promoted cell proliferation was mediated by PDCD4 and miR-4262 can activate the NF-κB pathway to promote the accumulation of nuclear NF-κB/P65. All of these findings suggested miR-4262 may play a role in the development of HCC. |
| Databáze: | OpenAIRE |
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