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<p>Prostate cancer is estimated to contribute to over 35,000 deaths of men residing in the United States, with the majority fatality due to metastatic disease. CDC7 is a kinase that regulates DNA replication and is found elevated during neuroendocrine transdifferentiation in lung and prostate cancer. In this study, we demonstrate that CDC7 is highly expressed in treatment-resistant prostate cancer, with even higher levels observed in treatment-resistant prostate cancer with neuroendocrine phenotype (NEPC). We further identify CDC7 as a critical regulator of prostate tumorigenesis. Downregulation of CDC7 significantly reduces prostate cancer cells growth and invasion <i>in vitro</i> and silencing CDC7 suppresses prostate tumor growth <i>in vivo</i>. Furthermore, we demonstrate that the inhibition of CDC7 using TAK-931, a selective CDC7 inhibitor, significantly reduces the proliferation, migration, and invasion of aggressive prostate cancer cells. TAK-931 treated prostate cancer cells exhibit an abnormal cell cycle profile, suggesting that CDC7 inhibition induces replication stress and promotes apoptosis. Collectively, our findings demonstrate that CDC7 is a regulator of tumor progression in prostate cancer and represents new therapeutic target in advanced prostate cancer.</p>

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CDC7 is a targetable regulator of advanced prostate cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月18日

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  • Alifiani B. Hartono,
  • HyeonJi Hwang,
  • Sidharth Paparaju,
  • Shiqin Liu,
  • James D. Brooks,
  • Eva Corey,
  • Tanya Stoyanova

摘要

Prostate cancer is estimated to contribute to over 35,000 deaths of men residing in the United States, with the majority fatality due to metastatic disease. CDC7 is a kinase that regulates DNA replication and is found elevated during neuroendocrine transdifferentiation in lung and prostate cancer. In this study, we demonstrate that CDC7 is highly expressed in treatment-resistant prostate cancer, with even higher levels observed in treatment-resistant prostate cancer with neuroendocrine phenotype (NEPC). We further identify CDC7 as a critical regulator of prostate tumorigenesis. Downregulation of CDC7 significantly reduces prostate cancer cells growth and invasion in vitro and silencing CDC7 suppresses prostate tumor growth in vivo. Furthermore, we demonstrate that the inhibition of CDC7 using TAK-931, a selective CDC7 inhibitor, significantly reduces the proliferation, migration, and invasion of aggressive prostate cancer cells. TAK-931 treated prostate cancer cells exhibit an abnormal cell cycle profile, suggesting that CDC7 inhibition induces replication stress and promotes apoptosis. Collectively, our findings demonstrate that CDC7 is a regulator of tumor progression in prostate cancer and represents new therapeutic target in advanced prostate cancer.