<HashMap><database>biostudies-literature</database><scores/><additional><submitter>He Z</submitter><funding>Medico- Engineering   Cooperation  Funds from  University  of  Electronic  Science and  Technology  of China</funding><funding>Medico- Engineering Cooperation Funds from University of Electronic Science and Technology of China</funding><funding>Foundation for Sichuan Provincial People’s Hospital</funding><funding>Foundation for Sichuan Provincial People's Hospital</funding><pagination>443</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9526964</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Gliomas account for about 80% of all malignant brain and other central nervous system (CNS) tumors. Temozolomide (TMZ) resistance represents a major treatment hurdle. Adrenomedullin (ADM) has been reported to induce glioblastoma cell growth.&lt;h4>Methods&lt;/h4>Cell viability was measured using the CCK-8 assay. The apoptosis analysis was performed using the Annexin V-FITC Apoptosis Detection Kit. The mitochondrial membrane potential was determined by JC-1 staining. A nude mouse tumor assay was used to detect tumor formation. Hematoxylin and eosin (H&amp;E) and immunohistochemical (IHC) staining were performed in tissue sections. Activation of Akt and Erk and expression of apoptosis-related proteins were determined by immunoblotting.&lt;h4>Results&lt;/h4>ADM expression has been found up</pubmed_abstract><journal>Journal of translational medicine</journal><pubmed_title>miR-1297 sensitizes glioma cells to temozolomide (TMZ) treatment through targeting adrenomedullin (ADM).</pubmed_title><pmcid>PMC9526964</pmcid><funding_grant_id>2021LY03</funding_grant_id><funding_grant_id>ZYGX2021YGLH209</funding_grant_id><pubmed_authors>Tang J</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>He Z</pubmed_authors><pubmed_authors>Hu J</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Cao D</pubmed_authors><pubmed_authors>Cheng M</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-1297 sensitizes glioma cells to temozolomide (TMZ) treatment through targeting adrenomedullin (ADM).</name><description>&lt;h4>Background&lt;/h4>Gliomas account for about 80% of all malignant brain and other central nervous system (CNS) tumors. Temozolomide (TMZ) resistance represents a major treatment hurdle. Adrenomedullin (ADM) has been reported to induce glioblastoma cell growth.&lt;h4>Methods&lt;/h4>Cell viability was measured using the CCK-8 assay. The apoptosis analysis was performed using the Annexin V-FITC Apoptosis Detection Kit. The mitochondrial membrane potential was determined by JC-1 staining. A nude mouse tumor assay was used to detect tumor formation. Hematoxylin and eosin (H&amp;E) and immunohistochemical (IHC) staining were performed in tissue sections. Activation of Akt and Erk and expression of apoptosis-related proteins were determined by immunoblotting.&lt;h4>Results&lt;/h4>ADM expression has been found up</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2025-04-19T11:32:37.824Z</modification><creation>2025-04-19T11:32:37.824Z</creation></dates><accession>S-EPMC9526964</accession><cross_references><pubmed>36183123</pubmed><doi>10.1186/s12967-022-03647-6</doi></cross_references></HashMap>