Apigenin suppresses proliferation, invasion, and epithelial-mesenchymal transition of cervical carcinoma cells by regulation of miR-152/BRD4 axis

The present study aimed to investigate the role of apigenin and the molecular mechanism of miR-152-5p and bromodomain containing 4 (BRD4) in the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of cervical carcinoma cells. Quantitative real-time PCR was used to detect the transfection efficiency and the expression of miR-152-5p and BRD4. Western blotting was conducted to evaluate the protein level of BRD4, E-cadherin, N-cadherin, and MMP9. Luciferase reporter assay was performed to confirm whether miR-152-5p bound to BRD4. MTT and Transwell invasion assay were applied to determine the cell proliferation and invasion, respectively. MiR-152-5p was downregulated and BRD4 was upregulated in cervical carcinoma tissue. Besides, miR-152-5p could directly bind to BRD4 in Hela and CaSki cells. In addition, apigenin inhibited proliferation, invasion, and EMT of Hela and CaSki cells by regulating miR-152-5p/BRD4 axis. Apigenin suppresses proliferation, invasion, and induced EMT of cervical carcinoma cells by regulation of miR-152-5p/BRD4 axis.

Automated summary

The study revealed that the expression levels of miR-152-5p and BRD4 in cervical carcinoma tissue are associated with cell proliferation, invasion, and EMT. Additionally, the findings showed that apigenin inhibits proliferation, invasion, and EMT of cervical carcinoma cells by regulating the miR-152-5p/BRD4 axis.