miR-31 Expression Correlates with Radiation-Induced Bystander Responses in Breast Cancer Cells

Mosavi Avendi, Seyedeh Simin; Ghanbarnasab-Behbahani, Rahil; Danyaei, Amir; Rasti, Mojtaba; Chegeni, Nahid

doi:10.31557/APJCP.2026.27.10.3699

miR-31 Expression Correlates with Radiation-Induced Bystander Responses in Breast Cancer Cells

Document Type : Research Articles

Authors

¹ Department of Medical Physics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

² Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

³ Infectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

10.31557/APJCP.2026.27.10.3699

Abstract

Purpose: This study investigated the association of miR-31 expression with radiation-induced bystander responses in non-irradiated MDA-MB-231 cells exposed to radiation-conditioned medium derived from irradiated MCF-7 breast cancer cells. Methods: MCF-7 cells were exposed to 0.5, 1, 2, and 4 Gy of 6 MV X-rays. Conditioned media were collected at 0, 24, and 48 hours’ post-irradiation and applied to MDA-MB-231 cells. Cell viability was assessed via MTT assay. Apoptosis and cell cycle behaviors were assessed using flow cytometry. Wound healing assays were conducted to assess migration, and RT-qPCR was used to quantify miR-31 expression. Results: MDA-MB-231 cells underwent dose- and time-dependent alterations associated with conditioned media from irradiated MCF-7 cells. Apoptosis increased significantly over time, especially in the 2 and 4 Gy groups. Cell cycle analysis showed shifts in the G1 and S phases. Migration rates were enhanced at specific time points, particularly in the 0.5 and 2 Gy groups. The expression of miR-31 was significantly increased in treated MDA-MB-231 cells. Conclusion: Our findings suggest a potential association between altered miR-31 expression and radiation-induced bystander responses in breast cancer cells. Further mechanistic studies are required to clarify its functional role and therapeutic relevance.

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