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Updated: Jun 16, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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STK32C promotes colon tumor progression through activating c-MYC signaling

Xin Zhang1, Mingxin Jin1, Yali Chu1

  • 1Department of General Surgery, Qilu Hospital of Shandong University, 107 West Wenhua Road, JiNan, 250012, China.

Cellular and Molecular Life Sciences : CMLS
|June 14, 2025
PubMed

Insights

Serine/threonine kinase 32C (STK32C) promotes colorectal cancer (CRC) progression by enhancing MYC signaling. Targeting STK32C may offer a new therapeutic strategy for CRC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Serine/threonine kinase 32C (STK32C) is an AGC kinase family member implicated in cancer progression.
  • The specific role of STK32C in colorectal cancer (CRC) and its underlying mechanisms are not well understood.

Purpose of the Study:

  • To investigate the role of STK32C in colorectal cancer (CRC) progression.
  • To elucidate the impact of STK32C on the MYC signaling pathway in CRC.

Main Methods:

  • Analysis of STK32C expression in CRC patient samples.
  • In vitro functional assays (proliferation, migration, invasion) in CRC cells.
  • In vivo mouse xenograft models to assess tumor growth.
  • Western blot analysis to evaluate MYC phosphorylation and stability.

Main Results:

  • STK32C expression is significantly upregulated in CRC tissues and correlates with poor prognosis.
  • STK32C promotes CRC cell proliferation, migration, and invasion.
  • STK32C enhances MYC stability and signaling by phosphorylating MYC at the S420 site.
  • STK32C knockdown suppresses tumor growth and MYC pathway activation in vivo.

Conclusions:

  • STK32C drives colorectal cancer progression through modulation of the MYC signaling pathway.
  • STK32C represents a potential therapeutic target for colorectal cancer treatment.
Keywords:
Colorectal cancerMYC signaling pathwaySTK32C

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