Research Article

Low-Dose Radiation-Induced Epithelial-Mesenchymal Transition (EMT) and Paracrine Pro-Invasive Magnification in MCF-7 Cells

Abstract

Background: Ionising radiation (IR) remains a cornerstone of breast cancer therapy, yet evidence indicates it can paradoxically promote malignant phenotypes in surviving cells. This study explored the contributions of direct irradiation versus exosome-mediated bystander signalling to epithelial-mesenchymal transition (EMT) and invasive potential in MCF-7 breast cancer cells under low dose of irradiation. Methods: MCF-7 cells were exposed to 0 Gy, 0.1 Gy, or 2 Gy X-ray irradiation, and invasion was quantified at early and late timepoints under direct irradiation and exosome-mediated bystander conditions. EMT markers (E-cadherin, Vimentin, N-cadherin, β-catenin) were assessed, and a Functional Invasion Efficiency Index (invasive cells per % N-cadherin) and Cadherin Switch Ratio (N-cadherin/β catenin) were calculated. Results: Direct irradiation produced a nonlinear response, peaking at 0.1 Gy (∼1.74-fold invasion) and plateauing at 2 Gy (∼4,800 cells/field). Exosome-mediated signalling drove progressive, dose-dependent escalation, reaching 11,385 cells/field at 2 Gy (late timepoint)—a 2.38-fold magnification over direct irradiation. The Functional Invasion Efficiency Index declined under direct irradiation (68.5→57.6) but surged with exosomes (70.3→129.7). Cadherin Switch Ratio increased dose-dependently (1.00→1.80 at 2 Gy), confirming EMT, though this was uncoupled from functional invasion under direct exposure. Conclusion: At clinically relevant radiation doses delayed sustained pro-invasive potentiation is the principal mechanism underlying bystander signalling and is mediated by exosomes which coordinate the upregulation of mesenchymal markers and invasion machinery. The results suggest that exosome-targeted approaches could be used in conjunction with radiotherapy, and also indicate the need for long-term monitoring after radiotherapy.

Authors affiliation:

Raheem Abd Zaid AL-Abedi (ORCID):  Department of Pathological Analysis, Faculty of Science, University of Kufa, Iraq; Department of Biomedical Science, Faculty of Health and Life Science, Oxford Brookes University, Oxford, UK.
Khalidah Ibrahim Taifor (ORCID): General Directorate of Education of Najaf Al-Ashraf, Najaf, Iraq.
Ammar Hassan Mayah (ORCID): Department of Biomedical Science, Faculty of Health and Life Science, Oxford Brookes University, Oxford, UK.
Susan A. Brooks (ORCID): Department of Biomedical Science, Faculty of Health and Life Science, Oxford Brookes University, Oxford, UK.
Munira Kadhim (ORCID): Department of Biomedical Science, Faculty of Health and Life Science, Oxford Brookes University, Oxford, UK.

How To Cite: R.A.Z. AL-Abedi, K.I. Taifor, A.H. Mayah, S.A. Brooks, and M. Kadhim. Low-Dose Radiation-Induced Epithelial-Mesenchymal Transition (EMT) and Paracrine Pro-Invasive Magnification in MCF-7 Cells. Journal of Biomedicine and Biosensors, 6(4):22–34, 2026. https://doi.org/10.58613/jbb645