<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jinesh GG</submitter><funding>NCI NIH HHS</funding><pagination>12371</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7378193</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>MYO18B has been proposed to contribute to the progression of hepatocellular carcinoma (HCC). However, the signals that govern MYO18B transcription are not known. Here we show that, a network of C19MC miRNA-520G, IFN-γ, CEBPB and p53 transcriptional-defects promote MYO18B mRNA expression in HCCs. IFN-γ by itself suppresses MYO18B transcription, but promotes it when miRNA-520G is stably overexpressed. Similarly, CEBPB-liver-enriched activator protein (LAP) isoform overexpression suppresses MYO18B transcription but promotes transcription when the cells are treated with IFN-γ. Furthermore, miR-520G together with mutant-p53 promotes MYO18B transcription. Conversely, bFGF suppresses MYO18B mRNA irrespective of CEBPB, miR-520G overexpression or IFN-γ treatment. Finally high MYO18B expression refl</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Regulation of MYO18B mRNA by a network of C19MC miRNA-520G, IFN-γ, CEBPB, p53 and bFGF in hepatocellular carcinoma.</pubmed_title><pmcid>PMC7378193</pmcid><funding_grant_id>R35 CA197452</funding_grant_id><pubmed_authors>Ackerman HD</pubmed_authors><pubmed_authors>Flores ER</pubmed_authors><pubmed_authors>Brohl AS</pubmed_authors><pubmed_authors>Napoli M</pubmed_authors><pubmed_authors>Jinesh GG</pubmed_authors><pubmed_authors>Raulji PM</pubmed_authors><pubmed_authors>Montey N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of MYO18B mRNA by a network of C19MC miRNA-520G, IFN-γ, CEBPB, p53 and bFGF in hepatocellular carcinoma.</name><description>MYO18B has been proposed to contribute to the progression of hepatocellular carcinoma (HCC). However, the signals that govern MYO18B transcription are not known. Here we show that, a network of C19MC miRNA-520G, IFN-γ, CEBPB and p53 transcriptional-defects promote MYO18B mRNA expression in HCCs. IFN-γ by itself suppresses MYO18B transcription, but promotes it when miRNA-520G is stably overexpressed. Similarly, CEBPB-liver-enriched activator protein (LAP) isoform overexpression suppresses MYO18B transcription but promotes transcription when the cells are treated with IFN-γ. Furthermore, miR-520G together with mutant-p53 promotes MYO18B transcription. Conversely, bFGF suppresses MYO18B mRNA irrespective of CEBPB, miR-520G overexpression or IFN-γ treatment. Finally high MYO18B expression refl</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2025-04-19T01:01:04.429Z</modification><creation>2025-04-07T11:57:20.091Z</creation></dates><accession>S-EPMC7378193</accession><cross_references><pubmed>32704163</pubmed><doi>10.1038/s41598-020-69179-5</doi></cross_references></HashMap>