<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Toledano S</submitter><funding>Israel Science Foundation</funding><pagination>41</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9852426</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>The semaphorin guidance factors receptor plexin-A2 transduces sema6A and sema6B signals and may mediate, along with plexin-A4, the anti-angiogenic effects of sema6A. When associated with neuropilins plexin-A2 also transduces the anti-angiogenic signals of sema3B. Here we show that inhibition of plexin-A2 expression in glioblastoma derived cells that express wild type p53 such as U87MG and A172 cells, or in primary human endothelial cells, strongly inhibits cell proliferation. Inhibition of plexin-A2 expression in U87MG cells also results in strong inhibition of their tumor forming ability. Knock-out of the plexin-A2 gene in U87MG cells using CRISPR/Cas9 inhibits cell proliferation which is rescued following plexin-A2 re-expression, or expression of a truncated plexin-A2 lacking its extrace</pubmed_abstract><journal>Cell death &amp; disease</journal><pubmed_title>Plexin-A2 enables the proliferation and the development of tumors from glioblastoma derived cells.</pubmed_title><pmcid>PMC9852426</pmcid><funding_grant_id>188/16</funding_grant_id><pubmed_authors>Kessler O</pubmed_authors><pubmed_authors>Neufeld G</pubmed_authors><pubmed_authors>Sabag AD</pubmed_authors><pubmed_authors>Liburkin-Dan T</pubmed_authors><pubmed_authors>Toledano S</pubmed_authors><pubmed_authors>Ilan N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Plexin-A2 enables the proliferation and the development of tumors from glioblastoma derived cells.</name><description>The semaphorin guidance factors receptor plexin-A2 transduces sema6A and sema6B signals and may mediate, along with plexin-A4, the anti-angiogenic effects of sema6A. When associated with neuropilins plexin-A2 also transduces the anti-angiogenic signals of sema3B. Here we show that inhibition of plexin-A2 expression in glioblastoma derived cells that express wild type p53 such as U87MG and A172 cells, or in primary human endothelial cells, strongly inhibits cell proliferation. Inhibition of plexin-A2 expression in U87MG cells also results in strong inhibition of their tumor forming ability. Knock-out of the plexin-A2 gene in U87MG cells using CRISPR/Cas9 inhibits cell proliferation which is rescued following plexin-A2 re-expression, or expression of a truncated plexin-A2 lacking its extrace</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-05-28T23:02:19.515Z</modification><creation>2024-10-16T17:14:28.294Z</creation></dates><accession>S-EPMC9852426</accession><cross_references><pubmed>36658114</pubmed><doi>10.1038/s41419-023-05554-0</doi></cross_references></HashMap>