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TRIM24-mediated K27-linked ubiquitination of ULK1 alleviates energy stress-induced autophagy and promote prostate cancer growth in the context of SPOP mutation

Cell Death & Differentiation (2025)Cite this article

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Abstract

SPOP, the most frequently mutated gene in prostate cancer, has been implicated in the aberrant activation of stress granules, presenting significant challenges in disease management. However, the mechanistic link between SPOP mutations and cellular energy stress remains inadequately explored. In this study, we demonstrate that ULK1 expression is positively correlated with both loss-of-function mutations in SPOP and the upregulation of the E3 ubiquitin ligase TRIM24 in human prostate cancer specimens. Mechanistically, SPOP mutations induce the upregulation of TRIM24, which subsequently binds to ULK1 and catalyzes its non-degradative K27-linked polyubiquitylation. This post-translational modification enhances the stability of ULK1, facilitating cellular adaptation to energy stress and consequently promoting prostate cancer progression. Notably, pharmacological inhibition of TRIM24 using TRIM24-PROTAC (proteolysis-targeting chimera) effectively suppressed tumor growth in mice bearing SPOP-mutant prostate cancer cells. Collectively, these findings elucidate a pivotal role of SPOP mutations in modulating energy stress responses via TRIM24-mediated ULK1 ubiquitylation and underscore the therapeutic potential of targeting TRIM24 in SPOP-mutant prostate cancers.

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Fig. 1: SPOP mutation facilitates autophagy under energy stress in prostate cancer.
Fig. 2: Regulation of ULK1 stability by SPOP mutation and TRIM24 expression.
Fig. 3: TRIM24 enhances ULK1 stability through interaction in SPOP-mutated prostate cancer.
Fig. 4: TRIM24’s B-box Domain Interacts with ULK1’s Spacer/CTD Domain to Mediate Polyubiquitylation.
Fig. 5: Disrupting SPOP mutation effects: therapeutic potential of dTRIM24 PROTAC in prostate cancer.
Fig. 6: Reduction of prostate carcinoma growth by dTRIM24 under energy-stressed conditions.
Fig. 7: The schematic diagram of the SPOP/TRIM24/ULK1 regulatory pathway.

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All data generated or analyzed during this study are included in this published article and its supplementary information files.

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Acknowledgements

The authors would like to express sincere gratitude to Cosmos Wisdom Company for their generous support and invaluable assistance throughout this research. The company’s technical support significantly contributed to the completion of this study. We deeply appreciate them for their support.

Funding

This work was supported by the National Natural Science Foundation of China (82372806 to LM, 82203450 to YZ, 82125026 to HR, 82472667 to ZY, 82188102 and 82030074 to ZL), the Ministry of Science and Technology of the People’s Republic of China (2020YFA0803300, ZL), the Natural Science Foundation of Shandong Province, China (ZR2021MC039 to LM), the Taishan Scholar Foundation of Shandong Province (tsqn202312378 to QW), Taishan Scholars Young Experts Project (tsqn202312380 to ZY) and Qingdao Key Clinical Specialty Elite Discipline. This work was supported by the Shanghai Sailing Program to YZ (20YF1448100 to YZ) and grants from the Science and Technology Commission of Shanghai Municipality (22Y11905200 to YZ).

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  1. These authors contributed equally: Shimin Chen, Jichun Lin, Zhan Yang.

Authors and Affiliations

  1. Department of Oncology, Cancer Institute of the Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer Institute, Qingdao, Shandong, China

    Shimin Chen, Jichun Lin, Yuanjing Wang, Dong Wang, Yue Qu, Qian Lin, Xue Li, Yinuo Chen, Wenshuo Fang, Jiaojiao Zhao & Leina Ma

  2. Oncology Department, Shandong Second Provincial General Hospital, Jinan, China

    Jichun Lin & Qiang Wang

  3. Shandong Provincial Key Laboratory of Clinical Research for Pancreatic Diseases, Tumor Immunology and Cytotherapy, Medical Research Center, The Affiliated Hospital of Qingdao University, Qingdao, China

    Zhan Yang & He Ren

  4. Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China

    Jia Liu

  5. Department of Urology, Shanghai Fourth People’s Hospital, School of Medicine, Tongji University, Shanghai, China

    Shi Yan

  6. College of Basic Medical Sciences, Naval Medical University, Shanghai, China

    Zixin Wang & Xueyu Qian

  7. Department of Urology, The First Affiliated Hospital, Naval Medical University, Shanghai, China

    Yutian Xiao & Yasheng Zhu

  8. Zhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China

    Zhimin Lu

  9. Institute of Fundamental and Transdisciplinary Research, Cancer Center, Zhejiang University, Hangzhou, China

    Zhimin Lu

  10. Gastrointestinal Cancer Institute/Pancreatic Disease Institute, the Affiliated Hospital of Qingdao University, Qingdao, Shandong, China

    He Ren

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Contributions

LM, YZ, DW, JLiu, QW, ZL, and HR. conceived and designed the study; LM, JLin, DW, QW, ZY, QL, SC, XL, WF, JZ, SY, ZW, XQ, YW, YQ, YC, and YX performed the experiments; JLiu, DW, YZ, and JLin performed the statistical analysis and wrote the original draft. LM, YZ, and HR contributed to the final draft. All authors contributed to the article and approved the submitted version.

Corresponding authors

Correspondence to Zhimin Lu, He Ren, Yasheng Zhu or Leina Ma.

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Chen, S., Lin, J., Yang, Z. et al. TRIM24-mediated K27-linked ubiquitination of ULK1 alleviates energy stress-induced autophagy and promote prostate cancer growth in the context of SPOP mutation. Cell Death Differ (2025). https://doi.org/10.1038/s41418-025-01582-9

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