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Purpose <p>The tumor microenvironment (TME) is a central regulator and driver of lung cancer progression. Within this TME, cancer-associated fibroblasts (CAFs) serve as key mediators of crosstalk between tumor cells and the surrounding stroma. CAFs promote immunosuppression, remodel the extracellular matrix (ECM), induce abnormal hypoxia and altered metabolism, and contribute to therapeutic resistance. These effects arise through dynamic interactions with cancer cells, cancer stem cells, and other stromal and immune components in the TME. Recent studies have revealed substantial heterogeneity among lung CAFs, with distinct subsets identified by specific marker proteins. This heterogeneity is associated with distinct secretory profiles that support tumor growth. </p> Method <p>The present review summarizes current understanding of the roles of CAFs in lung cancer progression and therapy resistance. </p> Results <p>We outline emerging strategies for targeting lung CAFs, including disrupting their signaling pathways, inhibiting ECM remodeling, and blocking CAF-derived secreted factors. In addition, we address the conflicting roles of CAFs in responses to immunotherapy, chemotherapy, and radiotherapy. </p> Conclusion <p>Finally, we discuss the therapeutic potential of novel approaches, including nanoparticle-based delivery systems, small-molecule inhibitors, natural compounds, and repurposed drugs.</p>

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Cancer-Associated Fibroblasts in Non-Small Cell Lung Carcinoma: Recent Progress and Future Perspectives on Potential Targets and Therapeutic Agents

  • 期刊论文

  • 发表日期：

    2026年2月27日

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  • Abdullah A. Aseeri,
  • Zahraa AlKhafaje,
  • Uday Abdul-Reda Hussein,
  • Zahraa Adel,
  • Ola Kamal A. Alkadir,
  • Ahmed Aldulaimi,
  • Shakir Mahmood Saeed,
  • Waam Mohammed Taher,
  • Mariem Alwan,
  • Aseel Smerat

摘要

Purpose

The tumor microenvironment (TME) is a central regulator and driver of lung cancer progression. Within this TME, cancer-associated fibroblasts (CAFs) serve as key mediators of crosstalk between tumor cells and the surrounding stroma. CAFs promote immunosuppression, remodel the extracellular matrix (ECM), induce abnormal hypoxia and altered metabolism, and contribute to therapeutic resistance. These effects arise through dynamic interactions with cancer cells, cancer stem cells, and other stromal and immune components in the TME. Recent studies have revealed substantial heterogeneity among lung CAFs, with distinct subsets identified by specific marker proteins. This heterogeneity is associated with distinct secretory profiles that support tumor growth.

Method

The present review summarizes current understanding of the roles of CAFs in lung cancer progression and therapy resistance.

Results

We outline emerging strategies for targeting lung CAFs, including disrupting their signaling pathways, inhibiting ECM remodeling, and blocking CAF-derived secreted factors. In addition, we address the conflicting roles of CAFs in responses to immunotherapy, chemotherapy, and radiotherapy.

Conclusion

Finally, we discuss the therapeutic potential of novel approaches, including nanoparticle-based delivery systems, small-molecule inhibitors, natural compounds, and repurposed drugs.