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Background <p>HOXB5, a member of the homeobox (HOX) gene family. Its dysregulated expression has been increasingly reported across multiple human cancers, where it correlates with malignant progression and poor clinical outcomes. A concise synthesis of its regulatory networks and cancer-associated functions is therefore needed to clarify its biological and translational significance.</p> Main body <p>This review summarizes the expression landscape of HOXB5 across diverse tumor types and delineates its key regulatory mechanisms, including noncoding RNAs, DNA methylation, histone modifications, phosphorylation events, HOX/PBX interactions, NPM1 mutations, RB1 loss, and single-nucleotide polymorphisms. Functionally, HOXB5 acts as a central regulatory node that integrates multiple signaling pathways to modulate cancer cell proliferation, migration, invasion, apoptosis, epithelial–mesenchymal transition (EMT), and remodeling of the tumor microenvironment. Notably, HOXB5 displays context-dependent dual functions in cancer, acting predominantly as an oncogene but serving as a tumor suppressor in specific settings. For example, HOXB5 can restrain tumor growth by driving B-cell conversion into tumor-specific T cells, while loss of the chromatin remodelers Arid4a/Arid4b reduces HOXB5 expression and may accelerate the progression of certain myeloid disorders to AML.</p> Conclusions <p>HOXB5 functions as either an oncogene or a tumor suppressor in a context-dependent manner, and it holds substantial potential as a diagnostic, prognostic, and therapeutic target.</p>

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HOXB5 in precision oncology: regulatory networks, functional duality, and clinical prospects

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月6日

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  • Kui Zhong,
  • Qiang Yi,
  • Zheng Chen,
  • Yongchang Xu,
  • Yangneng Zeng,
  • Jinghua Zhong

摘要

Background

HOXB5, a member of the homeobox (HOX) gene family. Its dysregulated expression has been increasingly reported across multiple human cancers, where it correlates with malignant progression and poor clinical outcomes. A concise synthesis of its regulatory networks and cancer-associated functions is therefore needed to clarify its biological and translational significance.

Main body

This review summarizes the expression landscape of HOXB5 across diverse tumor types and delineates its key regulatory mechanisms, including noncoding RNAs, DNA methylation, histone modifications, phosphorylation events, HOX/PBX interactions, NPM1 mutations, RB1 loss, and single-nucleotide polymorphisms. Functionally, HOXB5 acts as a central regulatory node that integrates multiple signaling pathways to modulate cancer cell proliferation, migration, invasion, apoptosis, epithelial–mesenchymal transition (EMT), and remodeling of the tumor microenvironment. Notably, HOXB5 displays context-dependent dual functions in cancer, acting predominantly as an oncogene but serving as a tumor suppressor in specific settings. For example, HOXB5 can restrain tumor growth by driving B-cell conversion into tumor-specific T cells, while loss of the chromatin remodelers Arid4a/Arid4b reduces HOXB5 expression and may accelerate the progression of certain myeloid disorders to AML.

Conclusions

HOXB5 functions as either an oncogene or a tumor suppressor in a context-dependent manner, and it holds substantial potential as a diagnostic, prognostic, and therapeutic target.