Introduction: Breast cancer (BC) is the most common female malignancy worldwide. For the definitive treatment of MC, radiotherapy can be used, as an important component, and uses ionizing radiation (IR). Studies reveal the potential capacity of IR to promote metastasis. The clinical response of BC to radiotherapy is related to radiosensitivity and resistance of irradiated cells, which is associated with clonogenic activity and sensitivity to radiation. Unsuccessful treatment increases the risk of local and distant recurrence.Methodology: Three breast cell lines (MCF-10A, MCF-7, and MDA-MB-231) were irradiated with 2 Gy and after 72 hours following markers were evaluated: E-cadherin, fibronectin, vimentin, and Snail. The processes of invasion, degradation of MMP2 and MMP9, and transendothelial migration were then assessed. Double-strand DNA breaks (DSBs), apoptosis, and colony formation were quantified. Result: The detection of γH2AX histone of irradiated cells showed that MCF-10A non-tumor cell is more radiosensitive while the MDA-MB-231 tumor cell is more radioresistant. The dose 2 Gy altered the formation of colonies to any of the cell lines. Tumorigenic cells exhibited a markedly increase in apoptosis, 24 h after irradiation while MCF-10A cells only after 72 h. A single dose of 2 Gy does not induce changes in the cellular microenvironment that lead to changes in the mesenchymal epithelium in breast BC.Conclusion: A dose of 2 Gy induces apoptosis and consequently an alteration in cell survival. However, a single dose of 2 Gy does not induce changes in the cellular microenvironment that lead to changes in the mesenchymal epithelium.

Mammography is an essential breast cancer screening tool that uses low doses of ionizing radiation. Determining whether such exposures modulate cellular processes associated with epithelial plasticity remains important. This preliminary study investigated whether clinically relevant radiation doses (≈2.14 mGy per exposure) influence epithelial-mesenchymal transition (EMT)-associated markers and motility in breast cell lines. Human breast cell lines MCF-10A (non-tumorigenic), MCF-7 (luminal, ER⁺), and MDA-MB-231 (triple-negative) were exposed to single (2.14 mGy) or repeated (2.14 + 2.14 mGy) doses. Exposure was defined using a Monte Carlo-estimated glandular-equivalent dose derived from a breast-equivalent phantom under mammographic conditions. EMT-associated markers (E-cadherin, fibronectin, vimentin), collective migration, extracellular matrix invasion, MMP-2/9 activity, and transendothelial migration were assessed. Low-dose irradiation induced cell-specific modulation of EMT-associated markers and motility (p-values correspond to single and repeated exposures, respectively). In MCF-10A cells, E-cadherin expression decreased (p = 0.0025; p = 0.028). A fibronectin degradation pattern was observed under both regimens; however, total band quantification (220 kDa subunit plus smaller fragments) was unchanged. Collective migration increased modestly (p < 0.05), while invasion through a basement membrane matrix increased markedly (p < 0.0001), and MMP-9 activity decreased (p < 0.0001). In MCF-7 cells, irradiation increased fibronectin (p = 0.05, repeated doses), enhanced collective migration (p < 0.05; p < 0.001), abolished MMP-2 activity in controls (in both treatments), and reduced MMP-9 activity (p < 0.0001), without altering invasion. In MDA-MB-231 cells, vimentin expression was upregulated after repeated exposures (p = 0.0067), while fibronectin expression decreased (p = 0.035; p = 0.046). Matrix invasion increased after single and repeated exposures (p < 0.05; p < 0.0001), MMP-9 activity increased after single exposure (p < 0.0001), and transendothelial migration decreased after single and repeated exposures (p < 0.01; p < 0.0001), without changes in collective migration. MMP-2 activity was undetectable in MCF-10A and MDA-MB-231 cells. Mammography-equivalent radiation doses were associated with lineage-dependent modulation of EMT-associated markers and cellular motility in vitro, indicating context-dependent phenotypic effects of clinically relevant low-dose radiation.