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Verified CAS / Academic Author2 Decoded Studies

Prof. CHEN Hongxiang

Shenzhen University Health Science Center / Huazhong University of Science and Technology Union Shenzhen Hospital

Research Publications & English Decoded Briefs

Showing 2 publications
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025063

FOXD3 promotes homologous recombination repair and genomic stability by facilitating MRE11-mediated DNA end resection

Homologous recombination (HR) is crucial for the high-fidelity repair of DNA double-strand breaks (DSBs), ensuring the maintenance of genome stability. In this study, we show that FOXD3 interacts with poly (ADP-ribose) polymerase 1 (PARP1) and is recruited to DSBs in a PARP1-dependent manner. FOXD3 directly binds to the DSB repair protein MRE11 and promotes its recruitment to DSB sites, ensuring proper end resection. Inhibition of FOXD3 expression compromises HR-mediated DSB repair and chromosome stability and sensitizes cancer cells to ionizing radiation. Collectively, our findings demonstrate that FOXD3 promotes HR-mediated DSB repair and genome stability.

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Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025063

FOXD3 promotes homologous recombination repair and genomic stability by facilitating MRE11-mediated DNA end resection

Homologous recombination (HR) is the high-fidelity pathway for repairing DNA double-strand breaks (DSBs) during S/G2 phases, and its dysfunction drives genomic instability and cancer progression. The MRN complex (MRE11/RAD50/NBS1) initiates DNA end resection, a critical step for HR, but how MRE11 recruitment and activity are regulated remains incompletely defined. Here we identify FOXD3 as a novel HR factor that interacts with PARP1 and is recruited to DSB sites in a PARP1-dependent manner. FOXD3 directly binds MRE11 and promotes its recruitment to DSBs, ensuring proper end resection. Depletion of FOXD3 impairs HR-mediated DSB repair, reduces chromosome stability, and sensitizes cancer cells to ionizing radiation. These findings establish FOXD3 as a key regulator of MRE11-mediated end resection and suggest that FOXD3 expression levels could serve as a biomarker for HR proficiency and as a therapeutic target to induce synthetic lethality with PARP inhibitors or radiotherapy. The study provides mechanistic insight into the early steps of HR and highlights the clinical potential of targeting FOXD3 in cancers with HR defects.

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