<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang B</submitter><funding>Natural Sciences and Engineering Research Council of Canada</funding><funding>Institute of Gender and Health</funding><funding>Alberta Cancer Foundation</funding><pagination>2876-2892</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6791708</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>18(21)</volume><pubmed_abstract>Glioblastoma is the most aggressive brain tumor. Although miR-141 has been demonstrated to primarily function as a tumor suppressor in numerous malignancies, including glioblastoma, the mechanisms involved remain poorly understood. Here, it is shown that miR-141 is downregulated in glioblastoma cell lines and tissues and may exert its biological function via directly targeting &lt;i>myelin transcription factor 1-like&lt;/i> (&lt;i>MYT1L&lt;/i>). Using two glioblastoma cell lines that differ from each other by the functionality of DNA-dependent protein kinase (DNAPK), a functional involvement of DNAPK in the miR-141 tumor suppression network was observed. In M059K cells with a normal function of DNAPK, the enforced expression of miR-141 attenuated MYT1L expression and suppressed cell proliferation. Con</pubmed_abstract><journal>Cell cycle (Georgetown, Tex.)</journal><pubmed_title>The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network.</pubmed_title><pmcid>PMC6791708</pmcid><funding_grant_id>N/A</funding_grant_id><funding_grant_id>05519</funding_grant_id><pubmed_authors>Rodriguez-Juarez R</pubmed_authors><pubmed_authors>Kovalchuk O</pubmed_authors><pubmed_authors>Ilnytskyy Y</pubmed_authors><pubmed_authors>Yao Y</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Li D</pubmed_authors><pubmed_authors>Kovalchuk I</pubmed_authors><pubmed_authors>Heyns M</pubmed_authors><pubmed_authors>Bronson RT</pubmed_authors><pubmed_authors>Kovalchuk A</pubmed_authors><pubmed_authors>Metz GAS</pubmed_authors></additional><is_claimable>false</is_claimable><name>The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network.</name><description>Glioblastoma is the most aggressive brain tumor. Although miR-141 has been demonstrated to primarily function as a tumor suppressor in numerous malignancies, including glioblastoma, the mechanisms involved remain poorly understood. Here, it is shown that miR-141 is downregulated in glioblastoma cell lines and tissues and may exert its biological function via directly targeting &lt;i>myelin transcription factor 1-like&lt;/i> (&lt;i>MYT1L&lt;/i>). Using two glioblastoma cell lines that differ from each other by the functionality of DNA-dependent protein kinase (DNAPK), a functional involvement of DNAPK in the miR-141 tumor suppression network was observed. In M059K cells with a normal function of DNAPK, the enforced expression of miR-141 attenuated MYT1L expression and suppressed cell proliferation. Con</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Nov</publication><modification>2025-04-22T10:36:16.206Z</modification><creation>2020-09-18T07:06:55Z</creation></dates><accession>S-EPMC6791708</accession><cross_references><pubmed>31522595</pubmed><doi>10.1080/15384101.2019.1652033</doi></cross_references></HashMap>