Upregulation of miR-206 attenuates breast cancer cell survival and increases their radiosensitivity.

Background: MicroRNAs (miRNAs) are a group of small non-coding RNAs that substantially participate in regulating gene expression. Their participation in cancer development encompasses various critical pathways, spanning from cell transformation to the progression of tumor cells, metastasis, and even resistance to treatment. This study aimed to assess the impact of miR-206 on radiosensitivity in breast cancer (BC) cells, SIRT1 activity, and p53 acetylation.

Method: miR-206 mimic or inhibitor was transfected into BC cell lines and exposed to X-ray radiation. MTT and colony-forming assays were used to estimate cell viability, and apoptosis was inspected using flow cytometry. SIRT1 enzymatic activity was assessed by a fluorescence method. The protein levels of p53 and its acetylation status were evaluated using western blotting. miR-206 levels were assessed in the breast tumor, marginal, and normal control tissue.

Results: The expression of miR-206 was significantly reduced in BC cell lines and tumor tissue compared to normal tissue. miR-206 reduced cell viability and induced apoptosis, and could enhance the suppressive effects of irradiation on cell viability, colony formation, and its ability to induce apoptosis. miR-206 effectively suppressed SIRT1 activity in BC cells. Moreover, miR-206 significantly increased the levels of p53 and its acetylated form.

Conclusion: The upregulation of miR-206 enhanced the efficacy of radiotherapy by promoting apoptosis and reducing cell survival. It also resulted in elevated levels of p53 and its acetylation. Therefore, miR-206 may be considered a promising candidate for radiosensitizing BC cells.