ArticleCell cycle (Georgetown, Tex.)2020
Diosmetin enhances the sensitivity of radiotherapy by suppressing homologous recombination in endometrial cancer.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Histone demethylase KDM4A promotes endometrial cancer progression through an ERRγ-associated cell-cycle regulatory axis.International journal of biological sciences · 2026Article
- Enhancement of doxorubicin efficacy by diosmetin through DNA damage accumulation and P-glycoprotein inhibition in breast cancer cells.Scientific reports · 2025Article
- Recent Advances in Diosmetin: Pharmacological, Pharmacokinetic, and Toxicological Profile.Current topics in medicinal chemistry · 2025Review
- Antitumor components and mechanisms ofFrontiers in pharmacology · 2025Review
- Construction of a prognostic model of luteolin for endometrial carcinoma.American journal of translational research · 2023Article
- Valproic Acid Regulates HR and Cell Cycle Through MUS81-pRPA2 Pathway in Response to Hydroxyurea.Frontiers in oncology · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
Radiotherapy is an essential treatment for endometrial cancer (EC), especially in advanced, metastatic, and recurrent cases. Combining radiotherapy, which mainly causes DNA double-strand breaks (DSBs), with small molecules targeting aberrantly activated homologous recombination (HR) repair pathways holds great potential for treating ECs in advanced stages. Here, we demonstrate that diosmetin (DIO), a natural flavonoid, suppresses HR, therefore inhibiting cell proliferation and enhancing the sensitivity of EC to radiotherapy. Clonogenic experiments revealed that combining DIO and X-ray significantly inhibited the viability of EC cells compared to cells treated with diosmetin or X-ray alone. The survival fraction of EC cells decreased to 40% when combining 0.4 Gy X-ray and 4 μM DIO; however, each treatment alone only caused death in approximately 15% and 22% of cancer cells, respectively. Further mechanistic studies showed that diosmetin inhibited the recruitment of RPA2 and RAD51, two critical factors involved in the HR repair pathway, upon the occurrence of DSBs. Thus, we propose that a combination of diosmetin and irradiation is a promising therapeutic strategy for treating endometrial cancer.
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