<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang H</submitter><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Institute of Neurological Disorders and Stroke</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Cancer Institute</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Heart, Lung, and Blood Institute</funding><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>422-435</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9345892</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>127(3)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Angiogenin is a multifunctional secreted ribonuclease that is upregulated in human cancers and downregulated or mutationally inactivated in neurodegenerative diseases. A role for angiogenin in glioblastoma was inferred from the inverse correlation of angiogenin expression with patient survival but had not been experimentally investigated.&lt;h4>Methods&lt;/h4>Angiogenin knockout mice were generated and the effect of angiogenin deficiency on glioblastoma progression was examined. Angiogenin and plexin-B2 genes were knocked down in glioblastoma cells and the changes in cell proliferation, invasion and vascular association were examined. Monoclonal antibodies of angiogenin and small molecules were used to assess the therapeutic activity of the angiogenin-plexin-B2 pathway in both</pubmed_abstract><journal>British journal of cancer</journal><pubmed_title>Angiogenin and plexin-B2 axis promotes glioblastoma progression by enhancing invasion, vascular association, proliferation and survival.</pubmed_title><pmcid>PMC9345892</pmcid><funding_grant_id>R01 HL135160</funding_grant_id><funding_grant_id>R01CA105241</funding_grant_id><funding_grant_id>R01NS065237</funding_grant_id><funding_grant_id>R01 CA105241</funding_grant_id><funding_grant_id>R01 NS065237</funding_grant_id><funding_grant_id>R01HL135160</funding_grant_id><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Jay D</pubmed_authors><pubmed_authors>Yuan L</pubmed_authors><pubmed_authors>Ibaragi S</pubmed_authors><pubmed_authors>Vanli N</pubmed_authors><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Hu AJ</pubmed_authors><pubmed_authors>Cochran B</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Kishikawa H</pubmed_authors><pubmed_authors>Shapiro R</pubmed_authors><pubmed_authors>Holland EC</pubmed_authors><pubmed_authors>Yu W</pubmed_authors><pubmed_authors>Goncalves KA</pubmed_authors><pubmed_authors>Hu GF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Angiogenin and plexin-B2 axis promotes glioblastoma progression by enhancing invasion, vascular association, proliferation and survival.</name><description>&lt;h4>Background&lt;/h4>Angiogenin is a multifunctional secreted ribonuclease that is upregulated in human cancers and downregulated or mutationally inactivated in neurodegenerative diseases. A role for angiogenin in glioblastoma was inferred from the inverse correlation of angiogenin expression with patient survival but had not been experimentally investigated.&lt;h4>Methods&lt;/h4>Angiogenin knockout mice were generated and the effect of angiogenin deficiency on glioblastoma progression was examined. Angiogenin and plexin-B2 genes were knocked down in glioblastoma cells and the changes in cell proliferation, invasion and vascular association were examined. Monoclonal antibodies of angiogenin and small molecules were used to assess the therapeutic activity of the angiogenin-plexin-B2 pathway in both</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2025-05-29T19:43:26.595Z</modification><creation>2025-05-29T19:43:26.595Z</creation></dates><accession>S-EPMC9345892</accession><cross_references><pubmed>35418212</pubmed><doi>10.1038/s41416-022-01814-6</doi></cross_references></HashMap>