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Background <p>Colorectal cancer (CRC) represents a prevalent global malignancy, with its progression intimately associated with biological processes such as oxidative stress and anoikis. This study aimed to evaluate a prognostic model derived from oxidative stress and anoikis-related genes (OARGs) in CRC and to elucidate the underlying mechanisms of the core gene, INHBB.</p> Results <p>We constructed a 12-genes prognostic model that retained independent predictive power for overall survival. Among the identified genes, INHBB was significantly upregulated in CRC tissues and cell lines, correlating with poor overall survival. Functional characterization revealed that INHBB overexpression markedly promoted malignant phenotypes, including proliferation, migration, and invasion. INHBB accelerates cell cycle progression, confers resistance to anoikis, exacerbates oxidative stress, and activates the epithelial-mesenchymal transition (EMT) pathway.</p> Conclusion <p>Beyond validating a novel OARGs-based prognostic model, this study highlights INHBB as a critical malignant regulator driving colorectal cancer aggressiveness, suggesting its potential as a prognostic biomarker and precision therapeutic target.</p> Clinical trial number <p>Not applicable.</p>

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High INHBB expression in colorectal cancer is associated with poor prognosis and drives malignant phenotypes in tumor cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月16日

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  • Huiyan Chen,
  • Yao Wu,
  • Zongxuan Huang,
  • Di Luo,
  • Ziming Wang,
  • Junhong Wu,
  • Tianyuan Zhou,
  • Hu Zhao

摘要

Background

Colorectal cancer (CRC) represents a prevalent global malignancy, with its progression intimately associated with biological processes such as oxidative stress and anoikis. This study aimed to evaluate a prognostic model derived from oxidative stress and anoikis-related genes (OARGs) in CRC and to elucidate the underlying mechanisms of the core gene, INHBB.

Results

We constructed a 12-genes prognostic model that retained independent predictive power for overall survival. Among the identified genes, INHBB was significantly upregulated in CRC tissues and cell lines, correlating with poor overall survival. Functional characterization revealed that INHBB overexpression markedly promoted malignant phenotypes, including proliferation, migration, and invasion. INHBB accelerates cell cycle progression, confers resistance to anoikis, exacerbates oxidative stress, and activates the epithelial-mesenchymal transition (EMT) pathway.

Conclusion

Beyond validating a novel OARGs-based prognostic model, this study highlights INHBB as a critical malignant regulator driving colorectal cancer aggressiveness, suggesting its potential as a prognostic biomarker and precision therapeutic target.

Clinical trial number

Not applicable.