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<p>Serine/threonine kinase 32C (STK32C) is a member of the AGC kinase family and has been identified as a potential promoter of cancer progression, though its role remains largely uncharacterized. This study explores the impact of STK32C on colorectal cancer (CRC) progression, particularly focusing on its influence on the MYC signaling pathway. Analysis of CRC samples and in vitro experiments revealed that STK32C expression is significantly elevated in cancerous tissues and associated with poor prognosis. Functional assays demonstrated that STK32C promotes proliferation, migration, and invasion of CRC cells, likely through phosphorylation of MYC at the S420 site, enhancing MYC stability and signaling activity. In vivo studies using a mouse xenograft model confirmed that STK32C knockdown suppresses tumor growth and MYC pathway activation. These findings suggest that STK32C contributes to CRC progression by modulating MYC signaling, highlighting its potential as a therapeutic target in CRC.</p>

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STK32C promotes colon tumor progression through activating c-MYC signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月14日

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  • Xin Zhang,
  • Mingxin Jin,
  • Yali Chu,
  • Fengjun Liu,
  • Hui Qu,
  • Cheng Chen

摘要

Serine/threonine kinase 32C (STK32C) is a member of the AGC kinase family and has been identified as a potential promoter of cancer progression, though its role remains largely uncharacterized. This study explores the impact of STK32C on colorectal cancer (CRC) progression, particularly focusing on its influence on the MYC signaling pathway. Analysis of CRC samples and in vitro experiments revealed that STK32C expression is significantly elevated in cancerous tissues and associated with poor prognosis. Functional assays demonstrated that STK32C promotes proliferation, migration, and invasion of CRC cells, likely through phosphorylation of MYC at the S420 site, enhancing MYC stability and signaling activity. In vivo studies using a mouse xenograft model confirmed that STK32C knockdown suppresses tumor growth and MYC pathway activation. These findings suggest that STK32C contributes to CRC progression by modulating MYC signaling, highlighting its potential as a therapeutic target in CRC.