Role of exosomal non‑coding RNAs in cancer‑associated fibroblast‑mediated therapy resistance (Review)

Junxin Li1, Yu Huang1, Lin Fu1

  • 1Department of Pharmacy, Zigong Fourth People's Hospital, Zigong, Sichuan 643000, P.R. China.

Insights

Cancer-associated fibroblasts (CAFs) and their exosomal RNAs are key players in cancer drug resistance. This review explores how CAFs and their non-coding RNAs influence therapeutic outcomes in the tumor microenvironment.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Cancer-associated fibroblasts (CAFs) are crucial stromal cells in the tumor microenvironment (TME).
  • Non-coding RNAs within exosomes mediate intercellular communication in the TME.
  • CAFs and exosomal RNAs significantly impact tumor progression and drug resistance.

Purpose of the Study:

  • To review the role of exosomal RNAs in CAF-mediated cancer therapeutic resistance.
  • To elucidate the mechanisms by which CAFs influence drug resistance via exosomal RNAs.
  • To provide recommendations for future research in CAF-induced drug resistance.

Main Methods:

  • Literature review of studies on CAFs, exosomes, and non-coding RNAs in cancer.
  • Analysis of mechanisms of intercellular communication involving exosomal RNAs between CAFs and cancer cells.
  • Synthesis of findings related to CAF-mediated modulation of therapeutic resistance.

Main Results:

  • Exosomal RNAs from cancer cells can activate CAFs, promoting cancer cell proliferation and invasion.
  • Exosomal RNAs from CAFs contribute to therapeutic resistance by affecting survival pathways, EMT, and immune evasion.
  • Specific non-coding RNAs within exosomes play critical roles in these interactions.

Conclusions:

  • Exosomal RNAs are vital mediators in the CAF-cancer cell communication axis.
  • Understanding these mechanisms is crucial for developing strategies to overcome CAF-driven therapeutic resistance.
  • Further research into specific exosomal RNA pathways is warranted to target CAF-mediated resistance effectively.

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