Assessing The Effects Of Mir-145 On The Radiosensitivity Of Breast Cancer Cells And The Underlying Molecular Mechanism

Purpose: To explore the contribution of miR-145 to the radiosensitivity of MDA-MB-231 cells and to understand the molecular mechanism. Methods: MDA-MB-231 cells were divided into a blank control group (BCG), a negative control group (NCG), and a miR-145-mimics group. qPCR was used to measure the expression of miR-145 and OCT4 mRNA at 48 h after transfection. A colony formation assay was used to determine the radiosensitivity of the transformed cells. Western blot analysis was conducted to assess OCT4, E-cadherin, and vimentin protein levels. MTT assay and flow cytometry were performed to evaluate proliferation and apoptosis, respectively, whereas a luciferase reporter assay was used to establish a correlation between miR-145 and OCT4. Results: miR-145 expression was downregulated in the MDA-MB-231 cells (P < 0.05), whereas miR-145 expression levels increased after transfection (P < 0.05). The miR-145-mimics group exhibited lower survival fraction, OCT4 mRNA and protein levels, vimentin levels, cell proliferation rate and higher E-cadherin protein levels and apoptosis than the other two groups (P < 0.05). The miR-145-mimics group exhibited lower luciferase activity with the 3 UTR gene vector of wildtype OCT4 than the NCG (P < 0.05). Group A exhibited lower OCT4 mRNA and protein levels and E-cadherin protein levels and higher vimentin levels and apoptosis than group B (P < 0.05). Conclusion: MiR-145 expression levels in breast cancer cells (BCCs) decreased. Overexpression of miR-145 induces epithelial-mesenchymal transition in BCCs, regulates cell proliferation and relocation, and increases radiosensitivity. These processes may be related to specific binding sites within the 3 UTR of OCT4.