PRRX2+ epithelial/SPP1+ macrophage crosstalk drives EMT and microenvironment remodeling in gemcitabine-resistant PDAC (IMAGE)
Caption
Schematic illustration of the proposed mechanism underlying gemcitabine resistance in pancreatic ductal adenocarcinoma. PRRX2 upregulation in malignant epithelial cells enhances TGF-β secretion, which activates TGF-β receptors on tumor-associated macrophages (TAMs), leading to increased SPP1 expression. Activated SPP1+ TAMs, in turn, promote epithelial–mesenchymal transition (EMT; VIM, FN1) and tumor microenvironment remodeling through factors such as MMP9, FN1, ITGA5, ANGPTL4, and VEGFA, thereby establishing an immunosuppressive and drug-resistant niche.
Credit
Chinese Medical Journal Image source link: https://journals.lww.com/cmj/fulltext/9900/single_cell_and_spatial_transcriptomics_reveal_the.1886.aspx
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