<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nakano M</submitter><funding>Kenichi Takano</funding><funding>Ryo Miyata</funding><funding>Takashi Kojima</funding><pagination>2584</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9179926</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The p53 family p63 is essential for the proliferation and differentiation of various epithelial basal cells. It is overexpressed in several cancers, including salivary gland neoplasia. Histone deacetylases (HDACs) are thought to play a crucial role in carcinogenesis, and HDAC inhibitors downregulate p63 expression in cancers.&lt;h4>Methods&lt;/h4>In the present study, to investigate the roles and regulation of p63 in salivary duct adenocarcinoma (SDC), human SDC cell line A253 was transfected with siRNA-p63 or treated with the HDAC inhibitors trichostatin A (TSA) and quisinostat (JNJ-26481585).&lt;h4>Results&lt;/h4>In a DNA array, the knockdown of p63 markedly induced mRNAs of the tight junction (TJ) proteins cingulin (CGN) and zonula occuludin-3 (ZO-3). The knockdown of p63 resulte</pubmed_abstract><journal>Cancers</journal><pubmed_title>Inhibition of HDAC and Signal Transduction Pathways Induces Tight Junctions and Promotes Differentiation in p63-Positive Salivary Duct Adenocarcinoma.</pubmed_title><pmcid>PMC9179926</pmcid><funding_grant_id>21K09610</funding_grant_id><funding_grant_id>19K18777</funding_grant_id><funding_grant_id>19K07464</funding_grant_id><pubmed_authors>Konno T</pubmed_authors><pubmed_authors>Kikuchi S</pubmed_authors><pubmed_authors>Kondoh A</pubmed_authors><pubmed_authors>Kojima T</pubmed_authors><pubmed_authors>Shindo Y</pubmed_authors><pubmed_authors>Ishii D</pubmed_authors><pubmed_authors>Kurose M</pubmed_authors><pubmed_authors>Nakano M</pubmed_authors><pubmed_authors>Takano K</pubmed_authors><pubmed_authors>Ohwada K</pubmed_authors><pubmed_authors>Obata K</pubmed_authors><pubmed_authors>Kohno T</pubmed_authors><pubmed_authors>Miyata R</pubmed_authors><pubmed_authors>Tsujiwaki M</pubmed_authors><pubmed_authors>Nishida S</pubmed_authors><pubmed_authors>Kakuki T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of HDAC and Signal Transduction Pathways Induces Tight Junctions and Promotes Differentiation in p63-Positive Salivary Duct Adenocarcinoma.</name><description>&lt;h4>Background&lt;/h4>The p53 family p63 is essential for the proliferation and differentiation of various epithelial basal cells. It is overexpressed in several cancers, including salivary gland neoplasia. Histone deacetylases (HDACs) are thought to play a crucial role in carcinogenesis, and HDAC inhibitors downregulate p63 expression in cancers.&lt;h4>Methods&lt;/h4>In the present study, to investigate the roles and regulation of p63 in salivary duct adenocarcinoma (SDC), human SDC cell line A253 was transfected with siRNA-p63 or treated with the HDAC inhibitors trichostatin A (TSA) and quisinostat (JNJ-26481585).&lt;h4>Results&lt;/h4>In a DNA array, the knockdown of p63 markedly induced mRNAs of the tight junction (TJ) proteins cingulin (CGN) and zonula occuludin-3 (ZO-3). The knockdown of p63 resulte</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2025-04-22T00:24:52.815Z</modification><creation>2024-11-08T13:21:11.786Z</creation></dates><accession>S-EPMC9179926</accession><cross_references><pubmed>35681564</pubmed><doi>10.3390/cancers14112584</doi></cross_references></HashMap>