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Stk10 Deficiency in Mice Promotes Tumor Growth by Dysregulating the Tumor Microenvironment

Jin-Xia Ma1, Dan-Dan Xu1, Shun-Yuan Lu1

  • 1Research Center for Experimental Medicine, State Key Laboratory of Medical Genomics, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Biology
|November 24, 2022
PubMed

Insights

Serine-threonine kinase 10 (STK10) influences prostate cancer growth by modulating immune cells in the tumor microenvironment. Deleting STK10 impairs anti-tumor immunity, increasing tumor growth and angiogenesis.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Serine-threonine kinase 10 (STK10), a STE20/p21-activated kinase (PAK) family member, is expressed in immune organs.
  • Previous studies indicated STK10's role in prostate cancer growth and metastasis.
  • The relationship between STK10 and the tumor microenvironment (TME) in prostate cancer is not well understood.

Purpose of the Study:

  • To investigate the association between STK10 and immune cells within the prostate cancer TME.
  • To determine the role of STK10 in tumor growth using a knockout mouse model.

Main Methods:

  • Bioinformatic analysis to assess STK10's relationship with tumor-infiltrating immune cells.
  • Utilizing an *Stk10* knockout mouse model to study tumor growth dynamics.

Main Results:

  • STK10 expression is significantly correlated with tumor-infiltrating lymphocytes, neutrophils, macrophages, and dendritic cells.
  • Deletion of host *Stk10* led to accelerated tumor growth.
  • This accelerated growth was associated with reduced activated/effector cytotoxic T lymphocytes (CTLs) and increased TME vessel density.

Conclusions:

  • Host STK10 plays a crucial role in the anti-tumor immune response.
  • STK10 modulates activated tumor-infiltrated CTLs and angiogenesis, impacting tumor progression.
Keywords:
CTLStk10angiogenesistumor microenvironment

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