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Background <p>K-homology-type splicing regulatory protein (KSRP) is an RNA-binding protein involved in mRNA decay and translational repression through recognition of adenine–uracil-rich elements. Although KSRP regulates approximately 16% of transcript expression, its role in cancer remains poorly defined.</p> Methods <p>KSRP expression was analysed using qPCR, Western blot, and immunohistochemistry. Its functional role in follicular thyroid cancer (FTC) was examined through in vitro and in vivo assays. Luciferase reporter and rescue experiments were performed to elucidate the underlying molecular mechanisms.</p> Results <p>KSRP was significantly upregulated in FTC tissues and metastatic cell lines. Functional studies demonstrated that KSRP enhances the invasiveness and stemness of FTC cells. Mechanistically, KSRP promotes nuclear accumulation and transcriptional activity of β-catenin by downregulating the Wnt inhibitors DACT2 and SFRP2.</p> Conclusion <p>This study identifies KSRP as an oncogenic factor in FTC that activates Wnt/β-catenin signalling, suggesting its potential as a therapeutic target for FTC patients.</p>

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KSRP-mediated Wnt/β-catenin activation promotes follicular thyroid cancer progression and stemness

  • 期刊论文

  • 发表日期：

    2025年8月23日

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  • Ke-Fan Pan,
  • Han-Lin Chou,
  • Wei-Li Wang,
  • Bo-Rong Chen,
  • Michael Hsiao,
  • Kuo-Tai Hua,
  • Ming-Hsun Wu

摘要

Background

K-homology-type splicing regulatory protein (KSRP) is an RNA-binding protein involved in mRNA decay and translational repression through recognition of adenine–uracil-rich elements. Although KSRP regulates approximately 16% of transcript expression, its role in cancer remains poorly defined.

Methods

KSRP expression was analysed using qPCR, Western blot, and immunohistochemistry. Its functional role in follicular thyroid cancer (FTC) was examined through in vitro and in vivo assays. Luciferase reporter and rescue experiments were performed to elucidate the underlying molecular mechanisms.

Results

KSRP was significantly upregulated in FTC tissues and metastatic cell lines. Functional studies demonstrated that KSRP enhances the invasiveness and stemness of FTC cells. Mechanistically, KSRP promotes nuclear accumulation and transcriptional activity of β-catenin by downregulating the Wnt inhibitors DACT2 and SFRP2.

Conclusion

This study identifies KSRP as an oncogenic factor in FTC that activates Wnt/β-catenin signalling, suggesting its potential as a therapeutic target for FTC patients.