{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang B"],"funding":["Natural Sciences and Engineering Research Council of Canada","Institute of Gender and Health","Alberta Cancer Foundation"],"pagination":["2876-2892"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6791708"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(21)"],"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 <i>myelin transcription factor 1-like</i> (<i>MYT1L</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"],"journal":["Cell cycle (Georgetown, Tex.)"],"pubmed_title":["The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network."],"pmcid":["PMC6791708"],"funding_grant_id":["N/A","05519"],"pubmed_authors":["Rodriguez-Juarez R","Kovalchuk O","Ilnytskyy Y","Yao Y","Wang B","Li D","Kovalchuk I","Heyns M","Bronson RT","Kovalchuk A","Metz GAS"],"additional_accession":[]},"is_claimable":false,"name":"The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network.","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 <i>myelin transcription factor 1-like</i> (<i>MYT1L</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","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Nov","modification":"2025-04-22T10:36:16.206Z","creation":"2020-09-18T07:06:55Z"},"accession":"S-EPMC6791708","cross_references":{"pubmed":["31522595"],"doi":["10.1080/15384101.2019.1652033"]}}