apoptree, Cancer associated fibroblast prolifer

apoptree,

Cancer associated fibroblast proliferation is complex, as with everything cancer associated.

However, fibroblast proliferation and accumulation is, at least in part, CCR5 driven.

Crucial involvement of the CCL3-CCR5 axis-mediated fibroblast accumulation in colitis-associated carcinogenesis in mice

https://onlinelibrary.wiley.com/doi/10.1002/ijc.28779

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Cancer-associated inflammatory responses consist of fibroblast accumulation as well as leukocyte infiltration.1 In order to prove the roles of fibroblast accumulation in this carcinogenesis model, we evaluated fibrotic changes in this colon carcinogenesis model. In mice given 4.5% DSS [dextran sulfate sodium], collagen deposition was increased in CCR1- but not CCL3- or CCR5-deficient mice as revealed by Masson's staining

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CCL3-CCR5 axis regulates intratumoral accumulation of leukocytes and fibroblasts and promotes angiogenesis in murine lung metastasis process
https://pubmed.ncbi.nlm.nih.gov/18941229/

Quote:

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CCL3- and CCR5-deficient mice exhibited a reduction in intratumoral accumulation of macrophages, granulocytes, and fibroblasts.

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Blockade of the chemokine receptor, CCR5, reduces the growth of orthotopically injected colon cancer cells via limiting cancer-associated fibroblast accumulation
https://pubmed.ncbi.nlm.nih.gov/27340784/

Quote:

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We previously demonstrated that cancer-associated fibroblasts (CAFs) accumulate at tumor sites through the interaction between a chemokine, CCL3, and its receptor, CCR5, in the late phase of colitis-associated colon carcinogenesis. Here we examined the effect of a CCR5 antagonist, maraviroc, on tumor growth arising from the orthotopic injection of mouse or human colon cancer cell lines into the cecal wall by focusing on CAFs. Orthotopic injection of either cell line caused tumor formation together with leukocyte infiltration and fibroblast accumulation. Concomitant oral administration of maraviroc reduced tumor formation with few effects on leukocyte infiltration. In contrast, maraviroc reduced the intratumor number of α-smooth muscle actin-positive fibroblasts, which express epidermal growth factor, a crucial growth factor for colon cancer cell growth. These observations suggest that maraviroc or other CCR5 antagonists might act as novel anti-CRC drugs to dampen CAFs, an essential cell component for tumor progression.

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Please forgive the mention of maraviroc.

I hope this is a helpful start.