The "Self-eating" of cancer-associated fibroblast: A potential target for cancer

Biomed Pharmacother. 2023 Jul:163:114762. doi: 10.1016/j.biopha.2023.114762. Epub 2023 Apr 24.

Abstract

Autophagy helps maintain energy homeostasis and protect cells from stress effects by selectively removing misfolded/polyubiquitylated proteins, lipids, and damaged mitochondria. Cancer-associated fibroblasts (CAFs) are cellular components of tumor microenvironment (TME). Autophagy in CAFs inhibits tumor development in the early stages; however, it has a tumor-promoting effect in advanced stages. In this review, we aimed to summarize the modulators responsible for the induction of autophagy in CAFs, such as hypoxia, nutrient deprivation, mitochondrial stress, and endoplasmic reticulum stress. In addition, we aimed to present autophagy-related signaling pathways in CAFs, and role of autophagy in CAF activation, tumor progression, tumor immune microenvironment. Autophagy in CAFs may be an emerging target for tumor therapy. In summary, autophagy in CAFs is regulated by a variety of modulators and can reshape tumor immune microenvironment, affecting tumor progression and treatment.

Keywords: Autophagy; Cancer; Cancer therapy; Cancer-associated fibroblast; Tumor immune microenvironment.

Publication types

  • Review

MeSH terms

  • Cancer-Associated Fibroblasts* / metabolism
  • Fibroblasts / metabolism
  • Humans
  • Mitochondria / metabolism
  • Neoplasms* / pathology
  • Signal Transduction
  • Tumor Microenvironment / physiology