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Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2.
- Source :
-
Artificial Cells, Nanomedicine & Biotechnology . Dec2019, Vol. 47 Issue 1, p2529-2535. 7p. - Publication Year :
- 2019
-
Abstract
- Objective: To investigate the regulatory mechanism of miR-204 on proliferation, apoptosis and autophagy of cervical cancer cells. Methods: The expression of miR-204 in cervical cancer tissues and cell lines was detected by real-time PCR. Cell viability and apoptosis were detected by MTT and flow cytometry, respectively. Protein expression of Bcl-2, Bax, Caspase-3 and LC3I/II in C33A cells after transfection was detected by Western blot assay. The interaction between miR-204 and ATF2 was verified by Targetscan online prediction, dual-luciferase assay and Western blot. Results: The expression of miR-204 was significantly down-regulated in cervical cancer tissues and cell lines (p <.05). Cell viability was suppressed while apoptosis was enhanced in C33A cells transfected with miR-204. In addition, overexpression of miR-204 reduced protein expression of Bcl-2 and LC3I/II and elevated protein expression of Bax and Caspase-3 in C33A cells (p <.05). The results of Targetscan online prediction, dual-luciferase assay and Western blot indicted that miR-204 could regulate the expression of ATF2. Cell viability was increased (p <.05) and the expression of ATF2 and LC3I/II was down-regulated (p <.05) in C33A cells after silencing of ATF2. Ectopic expression of ATF2 could restore miR-204 mediated inhibition on proliferation of C33A cells. Conclusions: miR-204 could inhibit proliferation and autophagy and induce apoptosis of cervical cancer cells by targeting ATF2, representing promising target for cervical cancer treatment. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 21691401
- Volume :
- 47
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Artificial Cells, Nanomedicine & Biotechnology
- Publication Type :
- Academic Journal
- Accession number :
- 141770417
- Full Text :
- https://doi.org/10.1080/21691401.2019.1628038