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Background <p>Collagen triple helix repeat containing 1 (CTHRC1) is an oncogene in numerous human cancers including oral squamous cell carcinoma (OSCC). However, whether and how CTHRC1 influences OSCC progression through ferroptosis has not been completely clarified.</p> Methods <p>qRT-PCR were conducted to assess CTHRC1 expression in OSCC. The proliferation of OSCC cells were assessed through 5-ethynyl-2’-deoxyuridine (EdU) assay, colony formation, and CCK-8 assays. Flow cytometry was used to analyze the apoptotic cells of OSCC cells. Ferroptosis was assessed based on the amounts of MDA, lipid ROS, intracellular Fe<sup>2+</sup>, and ferroptosis-related proteins. TGF-β/Smad pathway-related protein were detected by Western blot.</p> Results <p>Pronounced overexpression of CTHRC1 was observed in OSCC cell lines (SCC-9, CAL-27 and SCC-25). Knockdown CTHRC1 overtly inhibited cell proliferation but induced apoptosis in OSCC cells. Moreover, silencing of CTHRC1 could stimulate ferroptosis, as well as inhibit the activation of TGF-β/Smad pathway. Treatment with SRI-011381, a TGF-β/Smad pathway specific agonist, significantly reversed the promoting effect of CTHRC1 silencing on ferroptosis in OSCC cells.</p> Conclusions <p>Our findings indicate that knockdown of CTHRC1 stimulates ferroptosis in OSCC through inhibiting TGF-β/Smad pathway, which provides important experimental data and theoretical basis for the management, diagnosis, and treatment of OSCC.</p>

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CTHRC1/TGF-β/Smad axis serves as therapeutic targets in inhibiting oral squamous cell carcinoma by mediating ferroptosis

  • 期刊论文

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  • 发表日期：

    2025年12月25日

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  • Shihao Huang,
  • Yiming Jiao,
  • Yongchun Chang,
  • Yu Feng,
  • Guixian Mu,
  • Linli Xie

摘要

Background

Collagen triple helix repeat containing 1 (CTHRC1) is an oncogene in numerous human cancers including oral squamous cell carcinoma (OSCC). However, whether and how CTHRC1 influences OSCC progression through ferroptosis has not been completely clarified.

Methods

qRT-PCR were conducted to assess CTHRC1 expression in OSCC. The proliferation of OSCC cells were assessed through 5-ethynyl-2’-deoxyuridine (EdU) assay, colony formation, and CCK-8 assays. Flow cytometry was used to analyze the apoptotic cells of OSCC cells. Ferroptosis was assessed based on the amounts of MDA, lipid ROS, intracellular Fe2+, and ferroptosis-related proteins. TGF-β/Smad pathway-related protein were detected by Western blot.

Results

Pronounced overexpression of CTHRC1 was observed in OSCC cell lines (SCC-9, CAL-27 and SCC-25). Knockdown CTHRC1 overtly inhibited cell proliferation but induced apoptosis in OSCC cells. Moreover, silencing of CTHRC1 could stimulate ferroptosis, as well as inhibit the activation of TGF-β/Smad pathway. Treatment with SRI-011381, a TGF-β/Smad pathway specific agonist, significantly reversed the promoting effect of CTHRC1 silencing on ferroptosis in OSCC cells.

Conclusions

Our findings indicate that knockdown of CTHRC1 stimulates ferroptosis in OSCC through inhibiting TGF-β/Smad pathway, which provides important experimental data and theoretical basis for the management, diagnosis, and treatment of OSCC.