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Purpose of Review <p>Thrombospondin-2 (THBS2), an extracellular matrix (ECM) regulator, plays a multifaceted role in tumorigenesis. This review systematically summarizes recent advances regarding THBS2 in gastrointestinal tumors (including gastric, colorectal, pancreatic, and liver cancers) and evaluates its potential as a key player in the tumor microenvironment (TME), immune regulation, and clinical diagnostics and therapeutics.</p> Recent Findings <p>THBS2 promotes tumor proliferation and migration by activating the MAPK/PI3K/AKT pathway via integrins. It remodels the t TME through a TGF-β1-THBS2 feedback loop involving cancer-associated fibroblasts (CAFs). Furthermore, THBS2 facilitates metastasis and immune evasion by modulating ECM structure and cytoskeletal dynamics. Emerging therapeutic strategies aim to block THBS2 interactions with CD36/CD47 to enhance anti-PD-1 immunotherapy, disrupt the TGF-β-THBS2 signaling axis, or combine with matrix metalloproteinase (MMP) inhibitors to suppress fibrosis and tumor dissemination.</p> Summary <p> THBS2 acts as a critical regulator in the pathogenesis and progression of digestive tract tumors. Translating THBS2 into clinical practice requires addressing its context-dependent dual nature, tumor heterogeneity, and potential off-target resistance.</p>

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THBS2 as a Key Regulator in Gastrointestinal Tumors: from Molecular Mechanisms to Clinical Applications

  • 期刊论文

  • 发表日期：

    2026年2月5日

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  • Mengru Fang,
  • Mingyang Zou,
  • Haohua Deng,
  • Xiaoming Li,
  • Yajuan Zhu,
  • Wengui Shi,
  • Luxi Yang

摘要

Purpose of Review

Thrombospondin-2 (THBS2), an extracellular matrix (ECM) regulator, plays a multifaceted role in tumorigenesis. This review systematically summarizes recent advances regarding THBS2 in gastrointestinal tumors (including gastric, colorectal, pancreatic, and liver cancers) and evaluates its potential as a key player in the tumor microenvironment (TME), immune regulation, and clinical diagnostics and therapeutics.

Recent Findings

THBS2 promotes tumor proliferation and migration by activating the MAPK/PI3K/AKT pathway via integrins. It remodels the t TME through a TGF-β1-THBS2 feedback loop involving cancer-associated fibroblasts (CAFs). Furthermore, THBS2 facilitates metastasis and immune evasion by modulating ECM structure and cytoskeletal dynamics. Emerging therapeutic strategies aim to block THBS2 interactions with CD36/CD47 to enhance anti-PD-1 immunotherapy, disrupt the TGF-β-THBS2 signaling axis, or combine with matrix metalloproteinase (MMP) inhibitors to suppress fibrosis and tumor dissemination.

Summary

THBS2 acts as a critical regulator in the pathogenesis and progression of digestive tract tumors. Translating THBS2 into clinical practice requires addressing its context-dependent dual nature, tumor heterogeneity, and potential off-target resistance.