{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang R"],"funding":["National Natural Science Foundation of China"],"pagination":["97"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9977784"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Our previous studies have showed that C-C motif chemokine ligand 20 (CCL20) advanced tumor progression and enhanced the chemoresistance of cancer cells by positively regulating breast cancer stem cell (BCSC) self-renewal. However, it is unclear whether CCL20 affects breast cancer progression by remodeling the tumor microenvironment (TME). Here, we observed that polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) were remarkably enriched in TME of CCL20-overexpressing cancer cell orthotopic allograft tumors. Mechanistically, CCL20 activated the differentiation of granulocyte-monocyte progenitors (GMPs) via its receptor C-C motif chemokine receptor 6 (CCR6) leading to the PMN-MDSC expansion. PMN-MDSCs from CCL20-overexpressing cell orthotopic allograft tumors (CCL20-modulated PMN-"],"journal":["Signal transduction and targeted therapy"],"pubmed_title":["PMN-MDSCs modulated by CCL20 from cancer cells promoted breast cancer cell stemness through CXCL2-CXCR2 pathway."],"pmcid":["PMC9977784"],"funding_grant_id":["82073267","81930075"],"pubmed_authors":["Li F","Deng Q","Dong M","Zhang L","Liu S","Tu J","Ding J","Chang Z","Zhang R","Sheng D","Xu J","Ma W","Xia J","Dong H","Zhang Y","He X"],"additional_accession":[]},"is_claimable":false,"name":"PMN-MDSCs modulated by CCL20 from cancer cells promoted breast cancer cell stemness through CXCL2-CXCR2 pathway.","description":"Our previous studies have showed that C-C motif chemokine ligand 20 (CCL20) advanced tumor progression and enhanced the chemoresistance of cancer cells by positively regulating breast cancer stem cell (BCSC) self-renewal. However, it is unclear whether CCL20 affects breast cancer progression by remodeling the tumor microenvironment (TME). Here, we observed that polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) were remarkably enriched in TME of CCL20-overexpressing cancer cell orthotopic allograft tumors. Mechanistically, CCL20 activated the differentiation of granulocyte-monocyte progenitors (GMPs) via its receptor C-C motif chemokine receptor 6 (CCR6) leading to the PMN-MDSC expansion. PMN-MDSCs from CCL20-overexpressing cell orthotopic allograft tumors (CCL20-modulated PMN-","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-18T14:12:48.536Z","creation":"2025-04-07T00:13:52.844Z"},"accession":"S-EPMC9977784","cross_references":{"pubmed":["36859354"],"doi":["10.1038/s41392-023-01337-3"]}}