{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu C"],"funding":["the General Program of the Beijing Natural Science Foundation"],"pagination":["20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12908302"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["The tumor microenvironment (TME) has a profound influence on the progression of lung adenocarcinoma (LUAD) and its response to therapy. We identified a tumor-promoting communication network based on single-cell RNA sequencing. This shows an SPP1 + macrophage and basal epithelial cell communication module (CIM) that is enriched in invasive portions of tumors, and spatially associated with decreased cytotoxic T cell activity and poor prognosis. Transcriptomic modeling identified FAM117A as a major suppressor of the CIM network. FAM117A is a DYRK1A-interacting cell-cycle regulator. Loss of FAM117A resulted in longer G1/S transition time, increased cell proliferation, and an enhanced macrophage-epithelial feedback loop. Immunohistochemical studies showed decreased FAM117A expression in LUAD ti"],"journal":["Experimental hematology & oncology"],"pubmed_title":["Single-cell profiling reveals FAM117A as a key regulator linking macrophage-epithelial crosstalk with the progression of lung adenocarcinoma."],"pmcid":["PMC12908302"],"funding_grant_id":["7232164"],"pubmed_authors":["Liu H","Hu Y","Li D","Ren Z","Che G","Tao H","Wu C","Hou X","Wang J"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell profiling reveals FAM117A as a key regulator linking macrophage-epithelial crosstalk with the progression of lung adenocarcinoma.","description":"The tumor microenvironment (TME) has a profound influence on the progression of lung adenocarcinoma (LUAD) and its response to therapy. We identified a tumor-promoting communication network based on single-cell RNA sequencing. This shows an SPP1 + macrophage and basal epithelial cell communication module (CIM) that is enriched in invasive portions of tumors, and spatially associated with decreased cytotoxic T cell activity and poor prognosis. Transcriptomic modeling identified FAM117A as a major suppressor of the CIM network. FAM117A is a DYRK1A-interacting cell-cycle regulator. Loss of FAM117A resulted in longer G1/S transition time, increased cell proliferation, and an enhanced macrophage-epithelial feedback loop. Immunohistochemical studies showed decreased FAM117A expression in LUAD ti","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-16T05:05:15.792Z","creation":"2026-07-09T10:38:01.166Z"},"accession":"S-EPMC12908302","cross_references":{"pubmed":["41692823"],"doi":["10.1186/s40164-026-00745-9"]}}