<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11(3)</volume><submitter>Tang XY</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>The mechanisms involved in the malignant progression of lung adenocarcinoma (LUAD) are still inconclusive. Fibrinogen-like protein 1 (&lt;i>FGL1&lt;/i>) and &lt;i>LAG3&lt;/i> are a pair of immune checkpoints that create an inhibitory immune microenvironment in tumors. However, other roles of &lt;i>FGL1&lt;/i> in LUAD have not been extensively studied. Our study aims to explore the role of &lt;i>FGL1&lt;/i> in the malignant progression of LUAD and to provide new therapeutic targets and strategies for LUAD treatment.&lt;h4>Methods&lt;/h4>Differential gene expression of &lt;i>FGL1&lt;/i> was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA), Oncomine, UALCAN, and Gene Expression Omnibus (GEO) databases. A pan-cancer analysis was conducted using the Oncomine, TIMER, and UALCAN databases</pubmed_abstract><journal>Translational lung cancer research</journal><pagination>404-419</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8988074</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The downregulation of fibrinogen-like protein 1 inhibits the proliferation of lung adenocarcinoma via regulating &lt;i>MYC&lt;/i>-target genes.</pubmed_title><pmcid>PMC8988074</pmcid><pubmed_authors>Xiong YL</pubmed_authors><pubmed_authors>Han Q</pubmed_authors><pubmed_authors>Malhotra J</pubmed_authors><pubmed_authors>Zheng KF</pubmed_authors><pubmed_authors>Ma N</pubmed_authors><pubmed_authors>Lv Y</pubmed_authors><pubmed_authors>Jiang T</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Zhao JB</pubmed_authors><pubmed_authors>Liu YJ</pubmed_authors><pubmed_authors>Tang XY</pubmed_authors><pubmed_authors>Shi AP</pubmed_authors><pubmed_authors>Shi XG</pubmed_authors><pubmed_authors>Frattini M</pubmed_authors></additional><is_claimable>false</is_claimable><name>The downregulation of fibrinogen-like protein 1 inhibits the proliferation of lung adenocarcinoma via regulating &lt;i>MYC&lt;/i>-target genes.</name><description>&lt;h4>Background&lt;/h4>The mechanisms involved in the malignant progression of lung adenocarcinoma (LUAD) are still inconclusive. Fibrinogen-like protein 1 (&lt;i>FGL1&lt;/i>) and &lt;i>LAG3&lt;/i> are a pair of immune checkpoints that create an inhibitory immune microenvironment in tumors. However, other roles of &lt;i>FGL1&lt;/i> in LUAD have not been extensively studied. Our study aims to explore the role of &lt;i>FGL1&lt;/i> in the malignant progression of LUAD and to provide new therapeutic targets and strategies for LUAD treatment.&lt;h4>Methods&lt;/h4>Differential gene expression of &lt;i>FGL1&lt;/i> was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA), Oncomine, UALCAN, and Gene Expression Omnibus (GEO) databases. A pan-cancer analysis was conducted using the Oncomine, TIMER, and UALCAN databases</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-26T18:35:14.546Z</modification><creation>2024-11-21T11:07:46.893Z</creation></dates><accession>S-EPMC8988074</accession><cross_references><pubmed>35399566</pubmed><doi>10.21037/tlcr-22-151</doi></cross_references></HashMap>