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Article: Histone deacetylase 3 inhibits new tumor suppressor gene DTWD1 in gastric cancer

TitleHistone deacetylase 3 inhibits new tumor suppressor gene DTWD1 in gastric cancer
Authors
Ma, YYue, YPan, MSun, JChu, JLin, XXu, WFeng, LChen, YChen, DShin, VYWang, XJin, H
KeywordsHDAC
DTWD1
p53
gastric cancer
tumor suppressor gene
Issue Date2015
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us
Citation
American Journal of Cancer Research, 2015, v. 5 n. 2, p. 663-673 How to Cite?
AbstractCancer epigenetics plays an important role in the pathogenesis of many cancers including gastric cancer. Histone deacetylases (HDACs) emerge as exciting therapeutic targets for cancer treatment and prevention. In this study, we identified DTWD1 as one of the 122 genes upregulated after treatment of trichostatin A (TSA) in two gastric cancer cell lines. Moreover, DTWD1 was downregulated in gastric cancer cell lines and primary gastric carcinoma tissues. It was further identified as the new target of p53. Then we revealed that HDAC3 downregulated DTWD1 by disrupting the interaction of p53 with DTWD1 promoter. Furthermore, DTWD1 functioned as a tumor suppressor by downregulating cyclin B1 expression to inhibit proliferation. In summary, as the new p53 target gene, DTWD1 was downregulated in gastric cancer by HDAC3 and acted as a novel tumor suppressor gene. Specific inhibitors of HDAC3 might be a new approach for gastric cancer treatment by activating DTWD1 expression.
Persistent Identifierhttp://hdl.handle.net/10722/301137
ISSN
2156-6976
2021 Impact Factor: 5.942
2019 SCImago Journal Rankings: 1.562
PubMed Central ID
PMC4396045

 

DC FieldValueLanguage
dc.contributor.authorMa, Y-
dc.contributor.authorYue, Y-
dc.contributor.authorPan, M-
dc.contributor.authorSun, J-
dc.contributor.authorChu, J-
dc.contributor.authorLin, X-
dc.contributor.authorXu, W-
dc.contributor.authorFeng, L-
dc.contributor.authorChen, Y-
dc.contributor.authorChen, D-
dc.contributor.authorShin, VY-
dc.contributor.authorWang, X-
dc.contributor.authorJin, H-
dc.date.accessioned2021-07-27T08:06:40Z-
dc.date.available2021-07-27T08:06:40Z-
dc.date.issued2015-
dc.identifier.citationAmerican Journal of Cancer Research, 2015, v. 5 n. 2, p. 663-673-
dc.identifier.issn2156-6976-
dc.identifier.urihttp://hdl.handle.net/10722/301137-
dc.description.abstractCancer epigenetics plays an important role in the pathogenesis of many cancers including gastric cancer. Histone deacetylases (HDACs) emerge as exciting therapeutic targets for cancer treatment and prevention. In this study, we identified DTWD1 as one of the 122 genes upregulated after treatment of trichostatin A (TSA) in two gastric cancer cell lines. Moreover, DTWD1 was downregulated in gastric cancer cell lines and primary gastric carcinoma tissues. It was further identified as the new target of p53. Then we revealed that HDAC3 downregulated DTWD1 by disrupting the interaction of p53 with DTWD1 promoter. Furthermore, DTWD1 functioned as a tumor suppressor by downregulating cyclin B1 expression to inhibit proliferation. In summary, as the new p53 target gene, DTWD1 was downregulated in gastric cancer by HDAC3 and acted as a novel tumor suppressor gene. Specific inhibitors of HDAC3 might be a new approach for gastric cancer treatment by activating DTWD1 expression.-
dc.languageeng-
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us-
dc.relation.ispartofAmerican Journal of Cancer Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectHDAC-
dc.subjectDTWD1-
dc.subjectp53-
dc.subjectgastric cancer-
dc.subjecttumor suppressor gene-
dc.titleHistone deacetylase 3 inhibits new tumor suppressor gene DTWD1 in gastric cancer-
dc.typeArticle-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.authorityShin, VY=rp02000-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid25973305-
dc.identifier.pmcidPMC4396045-
dc.identifier.hkuros323792-
dc.identifier.volume5-
dc.identifier.issue2-
dc.identifier.spage663-
dc.identifier.epage673-
dc.publisher.placeUnited States-

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