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Related Experiment Video

Updated: Jan 13, 2026

Experimental Generation of Carcinoma-Associated Fibroblasts CAFs from Human Mammary Fibroblasts
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Cancer-Associated Fibroblasts Arising from Endothelial-to-Mesenchymal Transition: Induction Factors, Functional

Junyeol Han1,2, Eung-Gook Kim3, Bo Yeon Kim1,2

  • 1Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.

Biology
|October 29, 2025
PubMed
Summary

Endothelial-to-mesenchymal transition (EndMT) generates cancer-associated fibroblasts (CAFs) that drive tumor growth and therapy resistance. This review details EndMT induction methods and its impact on the tumor microenvironment (TME).

Keywords:
TGF-β signalingcancer-associated fibroblasts (CAF)endothelial-to-mesenchymal transition (EndMT)single-cell RNA sequencing (scRNA-seq)spatial transcriptomics sequencing (ST-seq)tumor microenvironment (TME)

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Related Experiment Videos

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Cancer-associated fibroblasts (CAFs) are crucial in the tumor microenvironment (TME), influencing cancer progression through extracellular matrix (ECM) remodeling and cytokine secretion.
  • Endothelial-to-mesenchymal transition (EndMT) is increasingly recognized as a significant contributor to the diverse origins of CAFs.

Purpose of the Study:

  • To review diverse methods for inducing EndMT in cancer models.
  • To summarize evidence of EndMT cell types using transcriptomic and proteomic data.
  • To discuss the mechanisms and consequences of cancer-induced EndMT on tumor progression and therapy resistance.

Main Methods:

  • Induction of EndMT in cancer-mouse tumor models via conditioned-medium treatment, co-culture, gene perturbation, ligand stimulation, exosome exposure, irradiation, viral infection, and 3D culture systems.
  • Transcriptomic and proteomic analyses to identify EndMT cell-type evidence.
  • Literature review of reported signaling pathways and cellular mechanisms involved in EndMT.

Main Results:

  • Hallmark EndMT features include altered morphology, increased motility, impaired angiogenesis, decreased endothelial markers (CD31, VE-cadherin), and increased mesenchymal markers (α-SMA, FN1).
  • Key signaling pathways implicated in EndMT include TGF-β, oxidative stress, and NOTCH signaling.
  • Cancer-induced EndMT promotes tumor growth, metastasis, expansion of cancer stem cells, macrophage differentiation, and is linked to poor survival and therapy resistance.

Conclusions:

  • EndMT is a critical process contributing to CAF heterogeneity and influencing tumor progression.
  • Understanding EndMT mechanisms and consequences is vital for developing novel cancer therapies.
  • Research perspectives differ on whether EndMT primarily generates CAFs or impacts endothelial barrier function and metastasis.