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Background <p>SUMO-specific peptidase 3 (SENP3), as a de-SUMOylating enzyme, renders the process of protein SUMOylation reversible. It has been demonstrated to play either promoting or inhibitory roles in several cancers. However, research on its function in colorectal cancer (CRC) remains absent.</p> Methods <p>Tissue samples from CRC patients were analyzed to measure the expression level of SENP3. Proliferation and viability assays were performed to assess the role of SENP3 in cell growth. The mouse model was established to evaluate the effect of SENP3 on the growth of xenografts derived from CRC cells. To investigate the mechanisms of SENP3 in CRC, proteomic analysis was conducted.</p> Results <p>We identified an elevated expression of SENP3 in cancerous tissues, which correlated with a reduced survival rate in CRC patients. SENP3 promoted cell growth in vitro and boosted tumorigenicity in vivo as a potential oncogenic factor. In terms of mechanism, proteomic analysis revealed that growth differentiation factor 15 (GDF15) is a downstream effector of SENP3. Treatment with MG132 confirmed that SENP3 enhances the stability of GDF15. Through a series of cellular functional experiments and mouse model establishment, we demonstrated that SENP3 regulates CRC progression by acting on GDF15.</p> Conclusion <p>Based on our findings, we define a key role for SENP3 in colorectal cancer progression and suggest it as a viable target for therapeutic intervention.</p>

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SENP3 drives colorectal cancer progression by enhancing GDF15 expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月13日

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  • Yang Yu,
  • Wenfang Bao,
  • Jingde Chen,
  • Yandong Li,
  • Yong Gao

摘要

Background

SUMO-specific peptidase 3 (SENP3), as a de-SUMOylating enzyme, renders the process of protein SUMOylation reversible. It has been demonstrated to play either promoting or inhibitory roles in several cancers. However, research on its function in colorectal cancer (CRC) remains absent.

Methods

Tissue samples from CRC patients were analyzed to measure the expression level of SENP3. Proliferation and viability assays were performed to assess the role of SENP3 in cell growth. The mouse model was established to evaluate the effect of SENP3 on the growth of xenografts derived from CRC cells. To investigate the mechanisms of SENP3 in CRC, proteomic analysis was conducted.

Results

We identified an elevated expression of SENP3 in cancerous tissues, which correlated with a reduced survival rate in CRC patients. SENP3 promoted cell growth in vitro and boosted tumorigenicity in vivo as a potential oncogenic factor. In terms of mechanism, proteomic analysis revealed that growth differentiation factor 15 (GDF15) is a downstream effector of SENP3. Treatment with MG132 confirmed that SENP3 enhances the stability of GDF15. Through a series of cellular functional experiments and mouse model establishment, we demonstrated that SENP3 regulates CRC progression by acting on GDF15.

Conclusion

Based on our findings, we define a key role for SENP3 in colorectal cancer progression and suggest it as a viable target for therapeutic intervention.