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Background <p>Angiogenesis is essential for colorectal cancer (CRC) progression. The role of serine/threonine kinase STK32C in this process remains unclear.</p> Methods <p>STK32C expression was examined in CRC tissues and correlated with patient prognosis. In vitro assays evaluated endothelial proliferation, migration, and tube formation. Mechanisms were studied using immunoprecipitation, western blotting, and gene set enrichment analysis. In vivo, xenograft and Matrigel plug assays assessed tumor growth and angiogenesis.</p> Results <p>STK32C was markedly overexpressed in CRC and associated with poor outcomes. Overexpression promoted endothelial angiogenic behaviors, while knockout suppressed them. Mechanistically, STK32C directly phosphorylated STAT3 at Thr196, enhancing its binding to JAK2 and activating IL-6/JAK2/STAT3 signaling. In vivo, STK32C depletion reduced tumor growth, VEGF-A expression, and microvessel density, confirming its pro-angiogenic function. STK32C-mediated tumor angiogenesis relied on STAT3 Thr196 phosphorylation.</p> Conclusions <p>STK32C acts as a pro-angiogenic driver in CRC by activating IL-6/JAK2/STAT3 signaling via STAT3 Thr196 phosphorylation. Its strong association with poor prognosis highlights STK32C as a potential biomarker and therapeutic target in anti-angiogenic therapy.</p>

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STK32C activated IL-6/JAK2/STAT3 signaling and promoted tumor angiogenesis

  • 期刊论文

  • 发表日期：

    2025年10月25日

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

摘要

Background

Angiogenesis is essential for colorectal cancer (CRC) progression. The role of serine/threonine kinase STK32C in this process remains unclear.

Methods

STK32C expression was examined in CRC tissues and correlated with patient prognosis. In vitro assays evaluated endothelial proliferation, migration, and tube formation. Mechanisms were studied using immunoprecipitation, western blotting, and gene set enrichment analysis. In vivo, xenograft and Matrigel plug assays assessed tumor growth and angiogenesis.

Results

STK32C was markedly overexpressed in CRC and associated with poor outcomes. Overexpression promoted endothelial angiogenic behaviors, while knockout suppressed them. Mechanistically, STK32C directly phosphorylated STAT3 at Thr196, enhancing its binding to JAK2 and activating IL-6/JAK2/STAT3 signaling. In vivo, STK32C depletion reduced tumor growth, VEGF-A expression, and microvessel density, confirming its pro-angiogenic function. STK32C-mediated tumor angiogenesis relied on STAT3 Thr196 phosphorylation.

Conclusions

STK32C acts as a pro-angiogenic driver in CRC by activating IL-6/JAK2/STAT3 signaling via STAT3 Thr196 phosphorylation. Its strong association with poor prognosis highlights STK32C as a potential biomarker and therapeutic target in anti-angiogenic therapy.