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<p>Chemotherapy resistance remains a major obstacle in breast cancer treatment. This study identifies DCAF13, a substrate recognition receptor of the CRL4 ubiquitin ligase complex, as a critical regulator of chemotherapy resistance through c-Myc-driven metabolic reprogramming. We found that DCAF13 expression was significantly upregulated in chemotherapy-resistant breast cancer cell lines compared to their parental counterparts. Inhibition of DCAF13 enhanced chemotherapy sensitivity, whereas its overexpression suppressed drug sensitivity. Mechanistically, DCAF13 upregulated c-Myc expression, driving metabolic reprogramming, characterized by increased glycolysis and oxidative phosphorylation. This metabolic shift promoted cell proliferation and resistance to chemotherapy. Clinically, DCAF13 expression correlated with poor prognosis in breast cancer patients, particularly in advanced stages and triple-negative breast cancer (TNBC). Our findings highlight the DCAF13-c-Myc axis as a critical mediator of chemotherapy resistance, suggesting that targeting this pathway could provide novel therapeutic strategies to overcome drug resistance in breast cancer. Further clinical studies are needed to explore the potential of DCAF13 as a therapeutic target.</p>

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DCAF13 influences breast cancer chemotherapy resistance through metabolic reprogramming by regulating c-Myc expression

  • 期刊论文

  • 发表日期：

    2025年4月23日

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  • Shiqiang Bai,
  • Yunlong Hu,
  • Ning Chen,
  • Liang Zhou,
  • Weiwei Ju,
  • Xinyi Qiao,
  • Jianyu Yu

摘要

Chemotherapy resistance remains a major obstacle in breast cancer treatment. This study identifies DCAF13, a substrate recognition receptor of the CRL4 ubiquitin ligase complex, as a critical regulator of chemotherapy resistance through c-Myc-driven metabolic reprogramming. We found that DCAF13 expression was significantly upregulated in chemotherapy-resistant breast cancer cell lines compared to their parental counterparts. Inhibition of DCAF13 enhanced chemotherapy sensitivity, whereas its overexpression suppressed drug sensitivity. Mechanistically, DCAF13 upregulated c-Myc expression, driving metabolic reprogramming, characterized by increased glycolysis and oxidative phosphorylation. This metabolic shift promoted cell proliferation and resistance to chemotherapy. Clinically, DCAF13 expression correlated with poor prognosis in breast cancer patients, particularly in advanced stages and triple-negative breast cancer (TNBC). Our findings highlight the DCAF13-c-Myc axis as a critical mediator of chemotherapy resistance, suggesting that targeting this pathway could provide novel therapeutic strategies to overcome drug resistance in breast cancer. Further clinical studies are needed to explore the potential of DCAF13 as a therapeutic target.