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miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2.
- Source :
-
International journal of molecular sciences [Int J Mol Sci] 2015 Jul 27; Vol. 16 (8), pp. 17018-28. Date of Electronic Publication: 2015 Jul 27. - Publication Year :
- 2015
-
Abstract
- Background: MiR-198 has been considered as an inhibitor of cell proliferation, invasion, migration and a promoter of apoptosis in most cancer cells, while its effect on non-cancer cells is poorly understood.<br />Methods: The effect of miR-198 transfection on HaCaT cell proliferation was firstly detected using Cell Count Kit-8 and the cell cycle progression was analyzed by flow cytometry. Using bioinformatics analyses and luciferase assay, a new target of miR-198 was searched and identified. Then, the effect of the new target gene of miR-198 on cell proliferation and cell cycle was also detected.<br />Results: Here we showed that miR-198 directly bound to the 3'-UTR of CCND2 mRNA, which was a key regulator in cell cycle progression. Overexpressed miR-198 repressed CCND2 expression at mRNA and protein levels and subsequently led to cell proliferation inhibition and cell cycle arrest in the G1 phase. Transfection ofSiCCND2 in HaCaT cells showed similar inhibitory effects on cell proliferation and cell cycle progression.<br />Conclusion: In conclusion, we have identified that miR-198 inhibited HaCaT cell proliferation by directly targeting CCND2.
- Subjects :
- 3' Untranslated Regions genetics
Base Sequence
Binding Sites
Cell Cycle Checkpoints genetics
Cell Line
Cell Proliferation
Cyclin D2 metabolism
Enzyme Assays
G1 Phase genetics
Humans
Luciferases metabolism
MicroRNAs genetics
Molecular Sequence Data
Protein Binding genetics
RNA, Messenger genetics
RNA, Messenger metabolism
RNA, Small Interfering metabolism
Transfection
Cyclin D2 genetics
Keratinocytes cytology
Keratinocytes metabolism
MicroRNAs metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1422-0067
- Volume :
- 16
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- International journal of molecular sciences
- Publication Type :
- Academic Journal
- Accession number :
- 26225959
- Full Text :
- https://doi.org/10.3390/ijms160817018