Further analysis revealed that EMT was an extremely significant mechanism regulated by CTHRC1 + GREM1 + myCAF (Fig. 3 e, f, Supplementary Fig. 2F ), indicating these fibroblasts support cancerous cell differentiation and proliferation leading to rapid tumor growth and potential metastasis.
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CTHRC1<sup>+</sup> fibroblasts and SPP1<sup>+</sup> macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma.
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