<HashMap><database>ENA</database><scores/><additional><omics_type>Genomics</omics_type><center_name>Jiangsu Cancer Hospital</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA1283220</full_dataset_link><scientific_name>Homo sapiens</scientific_name><long_description>The limited response rate to immune checkpoint inhibitors (ICIs) remains a significant challenge in the treatment of lung adenocarcinoma (LUAD). In our study, we identified a lactate-based chemical barrier surrounding FAP+ cancer-associated fibroblasts (CAFs) within the LUAD microenvironment (TME), which may hinder the infiltration and function of CD8+ T cells. Further investigation revealed that FAP+ CAFs specifically overexpress LINC01711. Hence, we performed RNA-seq in FAP+ CAFs, FAP- CAFs and FAP+ CAFs-siLINC01711, FAP+ CAFs-siNC cells. Overall design: Hence, we performed RNA-seq in FAP+ CAFs vs. FAP- CAFs and FAP+ CAFs-siLINC01711 vs. FAP+ CAFs-siNC cells.</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Targeting LINC01711 in FAP+ cancer-associated fibroblasts in lung adenocarcinoma</name><description>Targeting LINC01711 in FAP+ cancer-associated fibroblasts in lung adenocarcinoma</description><dates><last_updated>2025-09-24</last_updated><first_public>2025-07-04</first_public></dates><accession>PRJNA1283220</accession><cross_references><GEO>GSE301076</GEO><taxon>9606</taxon></cross_references></HashMap>