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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Updated: Sep 15, 2025

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Cancer-Associated Fibroblasts: Heterogeneity, Cancer Pathogenesis, and Therapeutic Targets.

Yutao Li1,2,3,4, Qingyun Liu1,2,3, Xilin Jing1,2,3,4

  • 1Department of Thoracic Surgery Peking University People's Hospital Beijing China.

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|July 14, 2025
PubMed
Summary

Cancer-associated fibroblasts (CAFs) are diverse cells that can either promote or inhibit tumor growth. Understanding CAF subtypes is key to developing targeted therapies that disrupt tumor-stroma coevolution and overcome resistance.

Keywords:
cancer‐associated fibroblastsheterogeneitypathogenesistheranostictumor microenvironment

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Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment Research

Background:

  • Cancer-associated fibroblasts (CAFs) are key stromal regulators in the tumor microenvironment (TME), influencing tumor progression, metastasis, and therapy resistance.
  • Recent single-cell multiomics and spatial transcriptomics reveal diverse CAF subtypes with context-dependent roles, capable of promoting immunosuppression or restraining tumor growth.
  • The functional duality of CAFs presents a challenge for developing effective therapeutic strategies.

Purpose of the Study:

  • To systematically categorize CAF subtypes based on origin, biomarkers, and TME-specific functions.
  • To review the roles of CAFs in chemoresistance, stemness maintenance, and immunosuppressive niche formation.
  • To evaluate emerging therapeutic strategies targeting CAFs and their signaling pathways.

Main Methods:

  • Systematic review and categorization of CAF subtypes.
  • Analysis of roles in chemoresistance, stemness, and immunosuppression.
  • Evaluation of emerging therapeutic strategies including selective depletion, epigenetic reprogramming, and pathway inhibition.

Main Results:

  • Identified conserved CAF subtypes with distinct molecular signatures and spatial distributions.
  • Highlighted the dual capacity of CAFs to promote immunosuppression or restrain tumor growth.
  • Evaluated targeting approaches like FAP+ CAF depletion and CXCL12/CXCR4 inhibition.

Conclusions:

  • Developing subtype-specific biomarkers and precision stromal therapies is crucial for disrupting tumor-stroma coevolution.
  • Spatial multiomics-driven combinatorial therapies, such as combining CAF targeting with immune checkpoint inhibitors, offer strategies to overcome microenvironment-driven resistance.
  • This review provides a roadmap for integrating CAF biology with translational advances for clinical innovation.