MiR-20a-5p suppressed TGF-β1-triggered apoptosis of human bronchial epithelial BEAS-2B cells by targeting STAT3.

Apoptosis of bronchial epithelial cells contributes to lung diseases, including asthma. Although miR-20a-5p is reportedly downregulated in the bronchial epithelia of asthmatic patients, its function and mechanism still need to be explored. Here, we explored how miR-20a-5p affects human bronchial epithelial cells stimulated with transforming growth factor (TGF)-β ₁ . Using qRT-PCR, we observed downregulated miR-20a-5p levels in these cells. After transfecting miR-20a-5p mimics or inhibitors into human bronchial epithelium BEAS-2B cells, a Cell Counting Kit-8 assay and flow cytometry analysis showed that the mimics mitigated suppression of cell viability and acceleration of apoptosis that was triggered by TGF-β ₁ , whereas the inhibitors exerted the opposite effects. TGF-β ₁ induced a decrease in expression of Bcl-2 and an increase in expression of Bax, both of which were inhibited by miR-20a-5p mimics and further enhanced by miR-20a-5p inhibitors. Further study verified that miR-20a-5p targeted the signal transducer and activator of transcription 3 (STAT3) and the STAT3 level was inversely related to the miR-20a-5p level. Furthermore, STAT3 overexpression partly counteracted the miR-20a-5p-induced anti-apoptotic effect in TGF-β1-treated BEAS-2B cells. In summary, this study suggested that miR-20a-5p restrained apoptosis in TGF-β1-stimulated BEAS-2B cells by targeting STAT3. MiR-20a-5p thus may be a novel therapeutic target for asthma treatment.
Competing Interests: Declaration of competing interest None.
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