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. 2022 Sep 7;5(4):889–901. doi: 10.20517/cdr.2022.67

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© The Author(s) 2022.

© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Targeting cancer-associated fibroblasts (CAFs) in cancer. Four main strategies targeting cancer-associated fibroblasts (CAFs) as cancer treatment are discussed. CAFs can be depleted by several treatments targeting CAF-specific markers, such as FAP and α-SMA. The normalization of CAFs from a pro-tumorigenic status to a quiescent or tumor-suppressive state can also be used for cancer treatment with small molecules such as ATRA or VDR ligands. The crucial signalings for CAF tumor-promoting function, such as cytokines and growth factors signalings, can be targeted to inactivate CAFs. Finally, CAF-derived extracellular matrix (ECM) proteins or related signalings can be targeted to induce ECM remodeling. MDSC: Myeloid-derived suppressor cell; FAP: fibroblast activation protein; CAR: chimeric antigen receptor; ATRA: all-trans retinoic acid; VDR: vitamin D receptor; FGFR: fibroblast growth factor receptor; SMO: smoothened; MMP: matrix metalloproteinase.