ArticleClinical and translational radiation oncology2026
MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53.
Article in Clinical and translational radiation oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Radiotherapy is one of the standard treatments for breast cancer, but its efficacy is limited by tumour radioresistance. Radiosensitizers can improve treatment outcomes. MonoHER, a flavonoid derivative, has shown anticancer potential; however, its role in radiosensitization has not been investigated. Here, we determined the radiosensitizing properties of monoHER in vitro in breast cancer and normal mammary cells. Methods: Breast cancer cells with different p53 status (MCF7, wild-type; T47D, mutant) and normal mammary cells (MCF10A) were treated with monoHER and radiation. Cell viability, clonogenic survival, apoptosis, and γ-H2AX foci were assessed. Western blotting examined ATM/p53 signalling. Interaction of monoHER with p53 was analysed by molecular docking and CETSA. Results: MonoHER selectively enhanced radiation-induced cytostatic effects in MCF7 (p < 0.01) cells and in T47D (p < 0.05), but had protective effect in MCF10A (p < 0.01) cells. Combined treatment increased apoptosis (p < 0.001) and DNA damage (p = 0.045) in MCF7 cells, accompanied by upregulation of p-ATM (p = 0.011), p-p53 (p = 0.023), and total p53 (p = 026), while in T47D and MCF10A cells, there is no significant difference. Docking and CETSA confirmed direct binding of monoHER to wild-type p53, increasing its thermal stability. MonoHER alone showed minimal cytotoxicity, suggesting a priming rather than direct killing effect. Conclusion: MonoHER modestly sensitize only p53-proficient breast cancer cells to radiation by stabilizing and activating p53, highlighting its potential as an adjuvant radiosensitizer.
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