1. Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2.
- Author
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Li N, Guo X, Liu L, Wang L, and Cheng R
- Subjects
- Adult, Cell Line, Tumor, Cell Proliferation genetics, Female, Gene Expression Regulation, Neoplastic genetics, Humans, Middle Aged, Activating Transcription Factor 2 genetics, Apoptosis genetics, Autophagy genetics, MicroRNAs genetics, Uterine Cervical Neoplasms genetics, Uterine Cervical Neoplasms pathology
- 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.
- Published
- 2019
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