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miR-503 inhibits proliferation making human hepatocellular carcinoma cells susceptible to 5‑fluorouracil by targeting EIF4E.
- Source :
-
Oncology reports [Oncol Rep] 2017 Jan; Vol. 37 (1), pp. 563-570. Date of Electronic Publication: 2016 Nov 07. - Publication Year :
- 2017
-
Abstract
- Hepatocellular carcinoma (HCC), a disease that is a major health care issue across the globe, includes the deviant expression of miRNAs in its development, progression, and resistance to treatment. We focused our study on miR‑503 expression and its role in HCC. miR‑503 was found in HCC tissues and cell lines using quantitative real-time PCR (RT‑qPCR). Western blot analyses and the luciferase reporter assay were used to determine the miR‑503 potential target in the HCC cells. We used MTT to analyze cell proliferation activity and noted that there was a considerable decrease of miR‑503 in HCC tissues and cell lines when measured against the controls. miR‑503 upregulation decreased expression of eukaryotic translation initiation factor 4E (EIF4E), and reduced HCC cell proliferation and sensitized HCC cells to anticancer drugs. miR‑503 overexpression hindered luciferase activity of EIF4E 3' untranslated region-based reporter construct among HepG2, BEL-7402, and SMMC-7721 cells, revealing that miR‑503 may increase sensitivity to therapies at least partially through targeting EIF4E suppression of HCC proliferation.
- Subjects :
- Carcinoma, Hepatocellular drug therapy
Carcinoma, Hepatocellular pathology
Cell Proliferation drug effects
Cells, Cultured
Down-Regulation drug effects
Down-Regulation genetics
Drug Resistance, Neoplasm genetics
Fluorouracil therapeutic use
Gene Expression Regulation, Neoplastic drug effects
Hep G2 Cells
Humans
Liver Neoplasms drug therapy
Liver Neoplasms pathology
Carcinoma, Hepatocellular genetics
Cell Proliferation genetics
Eukaryotic Initiation Factor-4E genetics
Liver Neoplasms genetics
MicroRNAs physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1791-2431
- Volume :
- 37
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Oncology reports
- Publication Type :
- Academic Journal
- Accession number :
- 27840964
- Full Text :
- https://doi.org/10.3892/or.2016.5220