SIRT1 inhibits proliferation of pancreatic cancer cells expressing pancreatic adenocarcinoma up-regulated factor (PAUF), a novel oncogene, by suppression of β-catenin

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dc.contributor.authorI R Cho-
dc.contributor.authorSang Seok Koh-
dc.contributor.authorW Malilas-
dc.contributor.authorR Srisuttee-
dc.contributor.authorJ Moon-
dc.contributor.authorY W Choi-
dc.contributor.authorY Horio-
dc.contributor.authorS Oh-
dc.contributor.authorY H Chung-
dc.date.accessioned2017-04-19T09:32:03Z-
dc.date.available2017-04-19T09:32:03Z-
dc.date.issued2012-
dc.identifier.issn0006-291X-
dc.identifier.uri10.1016/j.bbrc.2012.05.107ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10787-
dc.description.abstractBecause we found in a recent study that pancreatic adenocarcinoma up-regulated factor (PAUF), a novel oncogene, induces a rapid proliferation of pancreatic cells by up-regulation of β-catenin, we postulated that β-catenin might be a target molecule for pancreatic cancer treatment. We thus speculated whether SIRT1, known to target β-catenin in a colon cancer model, suppresses β-catenin in those pancreatic cancer cells that express PAUF (Panc-PAUF). We further evaluated whether such suppression would lead to inhibition of the proliferation of these cells. The ectopic expression of either SIRT1or resveratrol (an activator of SIRT1) suppressed levels of β-catenin protein and its transcriptional activity in Panc-PAUF cells. Conversely, suppression of SIRT1 expression by siRNA enhanced β-catenin expression and transcriptional activity. SIRT1 mutant analysis showed that nuclear localization of SIRT1 is not required for reduction of β-catenin. Treatment with MG132, a proteasomal inhibitor, restored β-catenin protein levels, suggesting that SIRT1-mediated degradation of β-catenin requires proteasomal activity. It was reported that inhibition of GSK-3β or Siah-1 stabilizes β-catenin in colon cancer cells, but suppression of GSK-3β or Siah-1 using siRNA in the presence of resveratrol instead diminished β-catenin protein levels in Panc-PAUF cells. This suggests that GSK-3β and Siah-1 are not involved in SIRT1-mediated degradation of β-catenin in the cells. Finally, activation of SIRT1 inhibited the proliferation of Panc-PAUF cells by down-regulation of cyclin-D1, a target molecule of β-catenin. These results suggest that SIRT1 activation may be a therapeutic strategy for treatment of pancreatic cancer cells that express PAUF via the down-regulation of β-catenin.-
dc.publisherElsevier-
dc.titleSIRT1 inhibits proliferation of pancreatic cancer cells expressing pancreatic adenocarcinoma up-regulated factor (PAUF), a novel oncogene, by suppression of β-catenin-
dc.title.alternativeSIRT1 inhibits proliferation of pancreatic cancer cells expressing pancreatic adenocarcinoma up-regulated factor (PAUF), a novel oncogene, by suppression of β-catenin-
dc.typeArticle-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.number2-
dc.citation.endPage275-
dc.citation.startPage270-
dc.citation.volume423-
dc.contributor.affiliatedAuthorSang Seok Koh-
dc.contributor.alternativeName조일래-
dc.contributor.alternativeName고상석-
dc.contributor.alternativeNameMalilas-
dc.contributor.alternativeNameSrisuttee-
dc.contributor.alternativeName문정-
dc.contributor.alternativeName최영환-
dc.contributor.alternativeNameHorio-
dc.contributor.alternativeName오상택-
dc.contributor.alternativeName정영화-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 423, no. 2, pp. 270-275-
dc.identifier.doi10.1016/j.bbrc.2012.05.107-
dc.subject.keywordβ-Catenin-
dc.subject.keywordPancreatic cancer-
dc.subject.keywordPAUF-
dc.subject.keywordSIRT1-
dc.subject.localβ-catenin-
dc.subject.localβ-Catenin-
dc.subject.localβcatenin-
dc.subject.localpancreatic cancer-
dc.subject.localPancreatic cancer-
dc.subject.localPAUF-
dc.subject.localSIRT-1-
dc.subject.localSIRT1-
dc.description.journalClassY-
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