<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Calanca N</submitter><funding>Conselho Nacional de Desenvolvimento Científico e Tecnológico</funding><funding>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil</funding><funding>Fundação de Amparo à Pesquisa do Estado de São Paulo</funding><funding>NCI NIH HHS</funding><pagination>741-750</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6615536</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(8)</volume><pubmed_abstract>Alternative protein-coding transcripts of the &lt;i>RASSF1&lt;/i> gene have been associated with dual functions in human cancer: while &lt;i>RASSF1C&lt;/i> isoform has oncogenic properties, &lt;i>RASSF1A&lt;/i> is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (&lt;i>ANRASSF1)&lt;/i> was implicated in a &lt;i>locus&lt;/i>-specific mechanism for the &lt;i>RASSF1A&lt;/i> epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of &lt;i>RASSF1A&lt;/i> and &lt;i>RASSF1C&lt;/i> and the expression levels of these &lt;i>RASSF1&lt;/i> transcripts in breast cancer and breast cancer cell lines. As expected, &lt;i>RASSF1C&lt;/i> remained unmethylated and &lt;i>RASSF1A&lt;/i> was hypermethylated at high frequencies in 75</pubmed_abstract><journal>Epigenetics</journal><pubmed_title>The long non-coding RNA &lt;i>ANRASSF1&lt;/i> in the regulation of alternative protein-coding transcripts &lt;i>RASSF1A&lt;/i> and &lt;i>RASSF1C&lt;/i> in human breast cancer cells: implications to epigenetic therapy.</pubmed_title><pmcid>PMC6615536</pmcid><funding_grant_id>Finance Code 001</funding_grant_id><funding_grant_id>CNPq Profix</funding_grant_id><funding_grant_id>FAPESP grant# 07/59110-9</funding_grant_id><funding_grant_id>P30 CA051008</funding_grant_id><pubmed_authors>Oliveira RA</pubmed_authors><pubmed_authors>Paschoal AP</pubmed_authors><pubmed_authors>Galindo LT</pubmed_authors><pubmed_authors>Munhoz EP</pubmed_authors><pubmed_authors>Caldeira JRF</pubmed_authors><pubmed_authors>Rogatto SR</pubmed_authors><pubmed_authors>Calanca N</pubmed_authors><pubmed_authors>Barbosa BM</pubmed_authors><pubmed_authors>Cavalli LR</pubmed_authors><pubmed_authors>Rainho CA</pubmed_authors></additional><is_claimable>false</is_claimable><name>The long non-coding RNA &lt;i>ANRASSF1&lt;/i> in the regulation of alternative protein-coding transcripts &lt;i>RASSF1A&lt;/i> and &lt;i>RASSF1C&lt;/i> in human breast cancer cells: implications to epigenetic therapy.</name><description>Alternative protein-coding transcripts of the &lt;i>RASSF1&lt;/i> gene have been associated with dual functions in human cancer: while &lt;i>RASSF1C&lt;/i> isoform has oncogenic properties, &lt;i>RASSF1A&lt;/i> is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (&lt;i>ANRASSF1)&lt;/i> was implicated in a &lt;i>locus&lt;/i>-specific mechanism for the &lt;i>RASSF1A&lt;/i> epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of &lt;i>RASSF1A&lt;/i> and &lt;i>RASSF1C&lt;/i> and the expression levels of these &lt;i>RASSF1&lt;/i> transcripts in breast cancer and breast cancer cell lines. As expected, &lt;i>RASSF1C&lt;/i> remained unmethylated and &lt;i>RASSF1A&lt;/i> was hypermethylated at high frequencies in 75</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Aug</publication><modification>2025-04-18T22:11:27.924Z</modification><creation>2020-05-30T07:02:25Z</creation></dates><accession>S-EPMC6615536</accession><cross_references><pubmed>31062660</pubmed><doi>10.1080/15592294.2019.1615355</doi></cross_references></HashMap>