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

Cho, Il-Rae; Koh, Sang Seok; Malilas, Waraporn; Srisuttee, Ratakorn; Moon, Jeong; Choi, Yang-Ho; Horio, Yoshiyuki; Oh, Sangtaek; Chung, Young‐Hwa

doi:10.1016/j.bbrc.2012.05.107

Cited by 46 publications

(48 citation statements)

References 31 publications

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“…The over-expression of SIRT1 inhibits prostate cancer cell lines [35] and pancreatic cancer cells [36]. While Zu, et al reported SIRT1 promotes proliferation of primary porcine aortic ECs measured by crystal violet [21], our results showed that the down-regulation of rat aortic EC proliferation is induced when SIRT1 is activated by either NSS or resveratrol, which is an activator doubled the rate of deacetylation by SIRT1 at about 11 µM [37].…”

Section: Discussionsupporting

confidence: 41%

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

Yao¹,

Qi²,

Zhang³

et al. 2013

Cell Physiol Biochem

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Background: Shear stress imposed by blood flow directly impacts endothelial cells (ECs), which are simultaneously influenced by neighboring vascular smooth muscle cells (VSMCs). However, the mechanisms by which shear stress and VSMCs modulate EC proliferation remain to be elucidated. Methods: ECs, cultured alone or co-cultured with VSMCs, were subjected to a normal level of laminar shear stress (NSS) of 15 dyne/cm² or kept under static conditions by using a parallel-plate flow chamber system, respectively. Results: BrdU incorporation assay and flow cytometry revealed that NSS inhibited EC proliferation with or without VSMCs. Western blot analysis demonstrated that NSS down-regulated the expression of Connexin40 (Cx40) in both ECs cultured alone and ECs co-cultured with VSMCs, accompanied by the increased expression of SIRT1. Moreover, salermide, an inhibitor of SIRT1, as well as SIRT1-specifc siRNA transfection inhibited the effect of NSS on EC proliferation and Cx40 expression. In contrast, resveratrol, a SIRT1 activator, induced an alteration in ECs similar to the application of NSS. Conclusion: NSS inhibits the proliferation of ECs via SIRT1 and Cx40 in the presence or absence of VSMCs. The data suggest that NSS plays a protective role in vascular homeostasis by maintaining EC proliferation at a normal level.

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Section: Discussionsupporting

confidence: 41%

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

Yao¹,

Qi²,

Zhang³

et al. 2013

Cell Physiol Biochem

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“…Detection of the mRNA levels of cyclin D1 revealed that SIRT1 inhibited the expression of cyclin D1 at the transcriptional level. Several transcription factors that bind the promoter of cyclin D1 gene have been proven to be inhibited by SIRT1, including NF-kB, b-catenin, and AP-1 (16,(34)(35)(36)(37). Among these three transcription factors, only NF-kB was inhibited by SIRT1 at the protein level.…”

Section: Discussionmentioning

confidence: 99%

SIRT1 Is Downregulated in Gastric Cancer and Leads to G1-phase Arrest via NF-κB/Cyclin D1 Signaling

Yang

Wang

Gao

et al. 2013

Molecular Cancer Research

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Sirtuin 1 (SIRT1) is a class III histone/protein deacetylase, and its activation status has been well documented to have physiologic benefits in human health. However, the function of SIRT1 in cancer remains controversial. Here, the expression and role of SIRT1 in gastric cancer is delineated. SIRT1 was present in all normal gastric mucosa specimens; however, it was only present in a portion of the matched gastric cancer tumor specimens. In SIRT1-positive tumors, both mRNA and protein levels were downregulated as compared with the corresponding nonneoplastic tissue. Ectopic expression of SIRT1 inhibited cell proliferation, diminished clonogenic potential, and induced a G 1 -phase cell-cycle arrest, the effects of which were not apparent when a catalytic-domain mutant form of SIRT1 was introduced, suggesting that SIRT1 functions in gastric cancer are dependent on its deacetylase activity. Further evidence was obtained from depletion of SIRT1. At the molecular level, SIRT1 inhibited the transcription of Cyclin D1 (CCND1), and inhibition of NF-kB in SIRT1-depleted cells rescued Cyclin D1 expression. Furthermore, inhibition of either NF-kB or Cyclin D1 in SIRT1-depleted cells reversed the inhibitory effects of SIRT1. The inhibitory role of SIRT1 was also verified in vivo using xenografts. This work characterizes SIRT1 status and demonstrates its inhibitory function in gastric cancer development, which involves NF-kB/ Cyclin D1 signaling, offering a therapeutic role for SIRT1 activators.

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“…Through its antioxidative properties, it has been shown to prevent or slow the progression of a wide variety of illnesses, including cardiovascular diseases, brain disorders, and cancer (Hung et al, 2000;Cho et al, 2012;Shin et al, 2012). In short-term type 1 diabetes, resveratrol was shown to improve cardiac function after ischemia-reperfusion injury by enhancing the anti-oxidative capacity of the heart (Thirunavukkarasu et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol, an activator of SIRT1, upregulates AMPK and improves cardiac function in heart failure

Gu¹,

Wang²,

Ye³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Reduced AMP-activated protein kinase (AMPK) expression has been shown to play a significant role in the cardiac dysfunction in heart failure. This study was designed to examine the effect of resveratrol, a potent activator of silent information regulator (SIRT1), on cardiac function and AMPK expression in heart failure. Adult male rat left anterior descending arteries were ligated, and they were fed with either a regular diet or a diet enriched with resveratrol. Heart failure was produced by myocardial infarction, and was associated with markedly increased AMPK and SIRT1 protein levels. Resveratrol treatment had a tremendous beneficial effect, both in terms of improving AMPK expression and on cardiac function. Decreased cardiac function and AMPK expression were also found in SIRT1 knockout (+/-) mice. In cultured cardiomyocytes, resveratrol increased AMPK and SIRT1 expressions, and overexpression of SIRT1 was found to be sufficient to activate AMPK in H9c2 cells. In contrast, pretreatment of cardiomyocytes with an SIRT1 antagonist, nicotinamide, blocked these beneficial effects of resveratrol. Therefore, the protective effects of resveratrol were found to be dependent on its ability to activate SIRT1 and improve AMPK expression. These results demonstrated that in heart failure, the enzymatic activity of cardiac SIRT1 is increased, which contributes to increased expression of AMPK, and resveratrol enhances the expression of AMPK and improves cardiac function through the activation of SIRT1.

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

Cited by 46 publications

References 31 publications

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

SIRT1 and Connexin40 Mediate the Normal Shear Stress-Induced Inhibition of the Proliferation of Endothelial Cells Co-Cultured with Vascular Smooth Muscle Cells

SIRT1 Is Downregulated in Gastric Cancer and Leads to G1-phase Arrest via NF-κB/Cyclin D1 Signaling

Resveratrol, an activator of SIRT1, upregulates AMPK and improves cardiac function in heart failure

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