1. MiRNA-211 triggers an autophagy-dependent apoptosis in cervical cancer cells: regulation of Bcl-2.
- Author
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Liu S, Wang H, Mu J, Wang H, Peng Y, Li Q, Mao D, and Guo L
- Subjects
- Adult, Biomarkers, Tumor biosynthesis, Biomarkers, Tumor genetics, Female, HeLa Cells, Humans, MicroRNAs genetics, Middle Aged, Proto-Oncogene Proteins c-bcl-2 genetics, Uterine Cervical Neoplasms genetics, Uterine Cervical Neoplasms pathology, Apoptosis physiology, Autophagy physiology, MicroRNAs biosynthesis, Proto-Oncogene Proteins c-bcl-2 biosynthesis, Uterine Cervical Neoplasms metabolism
- Abstract
Cervical cancer is a significant cause of morbidity and mortality in gynecological malignancies. Although autophagy plays a critical role in affecting cell apoptosis and proliferation, the role of hsa-miR-211-5p (miR-211) in modulating autophagy of cervical cancer cells remains unclear. In the current study, the level of miR-211 was downregulated in cervical cancer specimens, compared to the paired para-carcinoma tissues. While Bcl-2 was upregulated, LC3-II/I was decreased in the tumors, indicating inhibited apoptosis and autophagy. The forced expression of miR-211 inhibited proliferation, and promoted apoptosis in SiHa cervical cancer cells, evidenced by increased expression of apoptotic proteins, caspase-3, and PARP. While the miR-211 inhibitor exerted reverse effects on C-33A cervical cancer cells. Further, miR-211 induced autophagy in cervical cancer cells, as manifested by the presence of LC3 puncta, increased LC3-II/I and Beclin1 levels, and decreased p62 level. The miR-211-induced apoptosis was alleviated by an autophagy inhibitor 3-methyladenine (3-MA). In addition, Bcl-2 was identified as a target of miR-211. Besides, the apoptosis and autophagy triggered by miR-211 were attenuated by Bcl-2 in SiHa cells. In summary, our work indicates that miR-211 induced autophagy and autophagy-dependent apoptosis by regulating Bcl-2 in cervical cancer cells, which provided further understanding of autophagy in cervical carcinogenesis.
- Published
- 2020
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