{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xiao GY"],"funding":["HHS | NIH | National Cancer Institute","NCI NIH HHS","Cancer Prevention and Research Institute of Texas"],"pagination":["e2220276120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10334751"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(28)"],"pubmed_abstract":["Epithelial-to-mesenchymal transition (EMT) underlies immunosuppression, drug resistance, and metastasis in epithelial malignancies. However, the way in which EMT orchestrates disparate biological processes remains unclear. Here, we identify an EMT-activated vesicular trafficking network that coordinates promigratory focal adhesion dynamics with an immunosuppressive secretory program in lung adenocarcinoma (LUAD). The EMT-activating transcription factor ZEB1 drives exocytotic vesicular trafficking by relieving Rab6A, Rab8A, and guanine nucleotide exchange factors from miR-148a-dependent silencing, thereby facilitating MMP14-dependent focal adhesion turnover in LUAD cells and autotaxin-mediated CD8<sup>+</sup> T cell exhaustion, indicating that cell-intrinsic and extrinsic processes are link"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["EMT activates exocytotic Rabs to coordinate invasion and immunosuppression in lung cancer."],"pmcid":["PMC10334751"],"funding_grant_id":["R00 CA249048","P50 CA070907","P30 CA016672","P50 CA70907","R01 CA236781","R01 CA2111125","R01 CA211125","RP160652","K99 CA249048","R01 CA181184"],"pubmed_authors":["Haymaker C","Gibbons DL","Zhang J","Wistuba II","Xiao GY","Wu C","Rodriguez BL","Yu J","Xu J","Russell WK","Liu X","Kurie JM","Tan X","Solis L","Wang S","Vasquez ME","Lee Y","Tran HT"],"additional_accession":[]},"is_claimable":false,"name":"EMT activates exocytotic Rabs to coordinate invasion and immunosuppression in lung cancer.","description":"Epithelial-to-mesenchymal transition (EMT) underlies immunosuppression, drug resistance, and metastasis in epithelial malignancies. However, the way in which EMT orchestrates disparate biological processes remains unclear. Here, we identify an EMT-activated vesicular trafficking network that coordinates promigratory focal adhesion dynamics with an immunosuppressive secretory program in lung adenocarcinoma (LUAD). The EMT-activating transcription factor ZEB1 drives exocytotic vesicular trafficking by relieving Rab6A, Rab8A, and guanine nucleotide exchange factors from miR-148a-dependent silencing, thereby facilitating MMP14-dependent focal adhesion turnover in LUAD cells and autotaxin-mediated CD8<sup>+</sup> T cell exhaustion, indicating that cell-intrinsic and extrinsic processes are link","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-07-14T23:33:54.804Z","creation":"2025-04-06T14:50:52.106Z"},"accession":"S-EPMC10334751","cross_references":{"pubmed":["37406091"],"doi":["10.1073/pnas.2220276120"]}}