<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu X</submitter><funding>the Research Project of Jinan Microecological Biomedicine Shandong Laboratory</funding><funding>“20 Articles of Higher Education” Funding Project Independent Training Innovation Team of Jinan</funding><funding>University of Bergen</funding><funding>the Special Foundation for Taishan Scholars</funding><funding>the Clinical Research Center of Shandong University</funding><funding>National Natural Science Foundation of China</funding><funding>Central Guide Local Science and Technology Development Special Funds Projects</funding><funding>the Department of Science &amp;amp; Technology of Shandong Province</funding><pagination>147</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9960449</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Valtrate, a natural compound isolated from the root of Valeriana, exhibits antitumor activity in many cancers through different mechanisms. However, its efficacy for the treatment of glioblastoma (GBM), a tumor type with a poor prognosis, has not yet been rigorously investigated.&lt;h4>Methods&lt;/h4>GBM cell lines were treated with valtrate and CCK-8, colony formation and EdU assays, flow cytometry, and transwell, 3D tumor spheroid invasion and GBM-brain organoid co-culture invasion assays were performed to assess properties of proliferation, viability, apoptosis and invasion/migration. RNA sequencing analysis on valtrate-treated cells was performed to identify putative target genes underlying the antitumor activity of the drug in GBM cells. Western blot analysis, immunofluor</pubmed_abstract><journal>Journal of translational medicine</journal><pubmed_title>Valtrate, an iridoid compound in Valeriana, elicits anti-glioblastoma activity through inhibition of the PDGFRA/MEK/ERK signaling pathway.</pubmed_title><pmcid>PMC9960449</pmcid><funding_grant_id>81972351</funding_grant_id><funding_grant_id>2020CXGC010903</funding_grant_id><funding_grant_id>tshw201502056</funding_grant_id><funding_grant_id>JNL-2022042C</funding_grant_id><funding_grant_id>ZR2019ZD33</funding_grant_id><funding_grant_id>2020SDUCRCB002</funding_grant_id><funding_grant_id>tsqn201909173</funding_grant_id><funding_grant_id>YDZX2021010</funding_grant_id><funding_grant_id>2019GXRC006</funding_grant_id><funding_grant_id>JNL-2022003A</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Chen A</pubmed_authors><pubmed_authors>Hu Y</pubmed_authors><pubmed_authors>Wen M</pubmed_authors><pubmed_authors>Yang N</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Xue Z</pubmed_authors><pubmed_authors>Huang B</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Liu G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Valtrate, an iridoid compound in Valeriana, elicits anti-glioblastoma activity through inhibition of the PDGFRA/MEK/ERK signaling pathway.</name><description>&lt;h4>Background&lt;/h4>Valtrate, a natural compound isolated from the root of Valeriana, exhibits antitumor activity in many cancers through different mechanisms. However, its efficacy for the treatment of glioblastoma (GBM), a tumor type with a poor prognosis, has not yet been rigorously investigated.&lt;h4>Methods&lt;/h4>GBM cell lines were treated with valtrate and CCK-8, colony formation and EdU assays, flow cytometry, and transwell, 3D tumor spheroid invasion and GBM-brain organoid co-culture invasion assays were performed to assess properties of proliferation, viability, apoptosis and invasion/migration. RNA sequencing analysis on valtrate-treated cells was performed to identify putative target genes underlying the antitumor activity of the drug in GBM cells. Western blot analysis, immunofluor</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-05-28T19:01:49.53Z</modification><creation>2025-02-19T00:13:34.29Z</creation></dates><accession>S-EPMC9960449</accession><cross_references><pubmed>36829235</pubmed><doi>10.1186/s12967-023-03984-0</doi></cross_references></HashMap>