<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yu X</submitter><funding>Research Project of Jinan Microecological Biomedicine Shandong Laboratory</funding><funding>National Natural Science Foundation of China</funding><funding>Research Unit Project of Chinese Academy of Medical Sciences</funding><funding>Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences</funding><pagination>e2408788</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11923918</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(11)</volume><pubmed_abstract>Tumor-associated macrophages (TAMs) are commonly considered accomplices in tumorigenesis and tumor development. However, the precise mechanism by which tumor cells prompt TAMs to aid in evading immune surveillance remains to be further investigated. Here, it is elucidated that tumor-secreted galectin-1 (Gal1) conferred immunosuppressive properties to TAMs. Specifically, patient specimens and a public database is first used to analyze the clinical relevance of Gal1 in hepatocellular carcinoma (HCC). Then, it is demonstrated that TAMs functioned as a critical mediator in the Gal1-induced progression of HCC and the establishment of an immunosuppressive tumor microenvironment. Furthermore, RNA-sequencing determined that Gal1 promoted the upregulation of chemokine (C-C motif) ligand 20 (CCL20) </pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Galectin-1-Induced Tumor Associated Macrophages Repress Antitumor Immunity in Hepatocellular Carcinoma Through Recruitment of Tregs.</pubmed_title><pmcid>PMC11923918</pmcid><funding_grant_id>2023-PT320-02</funding_grant_id><funding_grant_id>2019-I2M-5-030</funding_grant_id><funding_grant_id>82172681</funding_grant_id><funding_grant_id>JNL-2022002A</funding_grant_id><pubmed_authors>Zhou L</pubmed_authors><pubmed_authors>Qian J</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Wu Q</pubmed_authors><pubmed_authors>Yin S</pubmed_authors><pubmed_authors>Zheng S</pubmed_authors><pubmed_authors>Ding L</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Su R</pubmed_authors><pubmed_authors>Pan C</pubmed_authors><pubmed_authors>Shang M</pubmed_authors><pubmed_authors>Xie H</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Guo D</pubmed_authors><pubmed_authors>Yu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Galectin-1-Induced Tumor Associated Macrophages Repress Antitumor Immunity in Hepatocellular Carcinoma Through Recruitment of Tregs.</name><description>Tumor-associated macrophages (TAMs) are commonly considered accomplices in tumorigenesis and tumor development. However, the precise mechanism by which tumor cells prompt TAMs to aid in evading immune surveillance remains to be further investigated. Here, it is elucidated that tumor-secreted galectin-1 (Gal1) conferred immunosuppressive properties to TAMs. Specifically, patient specimens and a public database is first used to analyze the clinical relevance of Gal1 in hepatocellular carcinoma (HCC). Then, it is demonstrated that TAMs functioned as a critical mediator in the Gal1-induced progression of HCC and the establishment of an immunosuppressive tumor microenvironment. Furthermore, RNA-sequencing determined that Gal1 promoted the upregulation of chemokine (C-C motif) ligand 20 (CCL20) </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2025-04-26T03:25:51.897Z</modification><creation>2025-04-06T10:49:04.486Z</creation></dates><accession>S-EPMC11923918</accession><cross_references><pubmed>39853961</pubmed><doi>10.1002/advs.202408788</doi></cross_references></HashMap>