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<p>One of the most prevalent malignant tumors in the male genitourinary system is prostate cancer (PCa). The health of men is seriously threatened by the lack of appropriate treatment options for advanced prostate cancer. As E3 ubiquitin ligases, the TRIM family is essential for the development and spread of tumors. Of them, TRIM27 plays a crucial role as a fundamental member of the TRIM family. The tumor immune microenvironment was closely linked to high expression of TRIM27, which was found to be an independent risk factor for a poor prognosis in PCa. Additional in vitro tests verified that TRIM27 stimulates the growth of tumors by controlling the expression of CANX by ubiquitination through triggering the PI3K/AKT signaling pathway. In the meantime, we used several transcription factor databases to find the transcription factor MYC, which can bind to the TRIM27 promoter region and increase its expression, in order to investigate the upstream regulators of TRIM27. In conclusion, our results show that MYC-regulated TRIM27 upregulation influences cancer development through CANX, offering new therapeutic targets and avenues for investigation in the detection and management of PCa.</p>

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MYC-driven TRIM27 upregulation promotes prostate cancer progression by enhancing CANX ubiquitination and activating PI3K/AKT signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Zitao Wang,
  • Jinzhuo Ning,
  • Lizhe Xu,
  • Fan Cheng

摘要

One of the most prevalent malignant tumors in the male genitourinary system is prostate cancer (PCa). The health of men is seriously threatened by the lack of appropriate treatment options for advanced prostate cancer. As E3 ubiquitin ligases, the TRIM family is essential for the development and spread of tumors. Of them, TRIM27 plays a crucial role as a fundamental member of the TRIM family. The tumor immune microenvironment was closely linked to high expression of TRIM27, which was found to be an independent risk factor for a poor prognosis in PCa. Additional in vitro tests verified that TRIM27 stimulates the growth of tumors by controlling the expression of CANX by ubiquitination through triggering the PI3K/AKT signaling pathway. In the meantime, we used several transcription factor databases to find the transcription factor MYC, which can bind to the TRIM27 promoter region and increase its expression, in order to investigate the upstream regulators of TRIM27. In conclusion, our results show that MYC-regulated TRIM27 upregulation influences cancer development through CANX, offering new therapeutic targets and avenues for investigation in the detection and management of PCa.