<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(18)</volume><submitter>Moraes L</submitter><pubmed_abstract>We previously reported that ABI3 expression was decreased in thyroid cancer tissues and that ectopic expression of ABI3 in a follicular thyroid carcinoma cell line delayed cell cycle progression and inhibited cell proliferation, invasion, migration and tumor formation in athymic mice. These data indicated that ABI3 is a tumor suppressor gene; however the mechanism through which ABI3 is silenced in thyroid carcinomas is unknown. We here show that treatment of four follicular thyroid carcinoma cell lines with 5-aza-dC induced demethylation of a specific region of the ABI3 promoter and restored ABI3 expression. In contrast, 5-aza-dC treatment did not restore ABI3 expression in a non-thyroid cell line, suggesting a tissue-specific regulation. We additionally show that 8 CpG sites located withi</pubmed_abstract><journal>Oncotarget</journal><pagination>25960-70</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5041957</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Transcriptional regulation of the potential tumor suppressor ABI3 gene in thyroid carcinomas: interplay between methylation and NKX2-1 availability.</pubmed_title><pmcid>PMC5041957</pmcid><pubmed_authors>Rubio I</pubmed_authors><pubmed_authors>Cerutti JM</pubmed_authors><pubmed_authors>Moraes L</pubmed_authors><pubmed_authors>Galrao AL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptional regulation of the potential tumor suppressor ABI3 gene in thyroid carcinomas: interplay between methylation and NKX2-1 availability.</name><description>We previously reported that ABI3 expression was decreased in thyroid cancer tissues and that ectopic expression of ABI3 in a follicular thyroid carcinoma cell line delayed cell cycle progression and inhibited cell proliferation, invasion, migration and tumor formation in athymic mice. These data indicated that ABI3 is a tumor suppressor gene; however the mechanism through which ABI3 is silenced in thyroid carcinomas is unknown. We here show that treatment of four follicular thyroid carcinoma cell lines with 5-aza-dC induced demethylation of a specific region of the ABI3 promoter and restored ABI3 expression. In contrast, 5-aza-dC treatment did not restore ABI3 expression in a non-thyroid cell line, suggesting a tissue-specific regulation. We additionally show that 8 CpG sites located withi</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 May</publication><modification>2026-04-16T09:22:09.541Z</modification><creation>2019-03-27T02:25:30Z</creation></dates><accession>S-EPMC5041957</accession><cross_references><pubmed>27036019</pubmed><doi>10.18632/oncotarget.8416</doi></cross_references></HashMap>