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<p>Fanconi anemia (FA) is primarily an autosomal recessive genetic disorder that leads to bone marrow failure, increased risk of developing cancer, and a plethora of developmental abnormalities. Patients are prone to recurrent infections and increased risk of hemorrhage, as well as delayed wound healing with poor results. FA is caused by a genetic mutation in the proteins needed for FA pathway activation; FA group D2 protein (FANCD2) is an indispensable part of this pathway and plays essential roles in some aspects of cellular life, especially in the cellular responses to DNA damage. Here, we found that depletion of FANCD2 induced reduction of proliferation and migration of NIH3T3 cells. Moreover, FANCD2 knockout decreased production of extracellular matrix (ECM) protein collagen III and cytoskeleton protein alpha-smooth muscle actin (α-SMA). In this process, FANCD2 knockout decreased the expression of DNA methyltransferase 1 (DNMT1), and DNMT1 inhibitor 5-aza-2′-deoxycytidine (5-AZA-CdR) also induced the decline of proliferation and migration ability of NIH3T3 cells, and reduced the expression of collagen III and α-SMA. These findings suggest that FANCD2 affects wound healing through DNMT1. These findings may provide novel therapeutic ideas for clinical treatment of patients with FA with poor wound healing.</p>

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FANCD2 promotes wound healing through DNMT1

  • 期刊论文

  • 发表日期：

    2026年1月13日

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  • Yingxiang Liu,
  • Jingjing Wang,
  • Hualong Lin,
  • Weijie Hao

摘要

Fanconi anemia (FA) is primarily an autosomal recessive genetic disorder that leads to bone marrow failure, increased risk of developing cancer, and a plethora of developmental abnormalities. Patients are prone to recurrent infections and increased risk of hemorrhage, as well as delayed wound healing with poor results. FA is caused by a genetic mutation in the proteins needed for FA pathway activation; FA group D2 protein (FANCD2) is an indispensable part of this pathway and plays essential roles in some aspects of cellular life, especially in the cellular responses to DNA damage. Here, we found that depletion of FANCD2 induced reduction of proliferation and migration of NIH3T3 cells. Moreover, FANCD2 knockout decreased production of extracellular matrix (ECM) protein collagen III and cytoskeleton protein alpha-smooth muscle actin (α-SMA). In this process, FANCD2 knockout decreased the expression of DNA methyltransferase 1 (DNMT1), and DNMT1 inhibitor 5-aza-2′-deoxycytidine (5-AZA-CdR) also induced the decline of proliferation and migration ability of NIH3T3 cells, and reduced the expression of collagen III and α-SMA. These findings suggest that FANCD2 affects wound healing through DNMT1. These findings may provide novel therapeutic ideas for clinical treatment of patients with FA with poor wound healing.