A novel role for the adipokine visfatin/pre-B cell colony-enhancing factor 1 in prostate carcinogenesis

Patel, Snehal; Mistry, Tına; Brown, James E.; Digby, Janet E.; Adya, Raghu; Desai, Ken; Randeva, Harpal S.

doi:10.1016/j.peptides.2009.10.001

Cited by 83 publications

(74 citation statements)

References 27 publications

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“…The present study showed that visfatin induced cell proliferation in HepG2 cells by activating PI3K and MAPK signaling pathways because visfatin stimulation significantly increased phosphorylation of Akt, ERK, and GSK-3b proteins in these cells. These findings are consistent with previous reports that visfatin regulates a variety of signaling pathways, including PI3K/Akt, MAPK/ERK, and Stat3 (20,32,33). Visfatin stimulation also increases cell proliferation and ERK activity in prostate cancer cells (20).…”

Section: Discussionsupporting

confidence: 93%

“…These findings are consistent with previous reports that visfatin regulates a variety of signaling pathways, including PI3K/Akt, MAPK/ERK, and Stat3 (20,32,33). Visfatin stimulation also increases cell proliferation and ERK activity in prostate cancer cells (20). Moreover, recent experimental studies have shown that the activation of PI3K/Akt, MAPK/ERK, and Stat3 pathways is , and induction of apoptosis in HepG2 cells in the presence and absence of visfatin.…”

Section: Discussionsupporting

confidence: 92%

“…Serum visfatin level is a good biomarker of colorectal malignant potential and stage progression (19). Visfatin stimulation increases cell proliferation in prostate and breast cancer cells (20,21), whereas the use of visfatin inhibitor exerts an antitumor effect by inducing apoptosis (22). These findings suggest that visfatin is one of the key adipocytokines that links obesity and tumorigenesis and thus may be an effective target for the inhibition of obesity-related carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Possible Role of Visfatin in Hepatoma Progression and the Effects of Branched-Chain Amino Acids on Visfatin-Induced Proliferation in Human Hepatoma Cells

Ninomiya

Shimizu

Imai

et al. 2011

Cancer Prevention Research

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Obesity and related metabolic abnormalities, including adipocytokine dysbalance, are risk factors for hepatocellular carcinoma (HCC). Visfatin, an adipocytokine that is highly expressed in visceral fat, is suggested to play a role in the progression of human malignancies. Branched-chain amino acids (BCAA) reduce the incidence of HCC in obese patients with liver cirrhosis and prevent obesity-related liver carcinogenesis in mice. In this study, we investigated the possible role of visfatin on HCC progression and the effects of BCAA on visfatin-induced proliferation of HCC cells. In patients with HCCs, serum visfatin levels were significantly correlated with stage progression and tumor enlargement. Visfatin preferentially stimulated the proliferation of HepG2, Hep3B, and HuH7 human HCC cells compared with Hc normal hepatocytes. Visfatin phosphorylated extracellular signal-regulated kinase (ERK), Akt, and GSK-3b proteins in HepG2 cells. LY294002 [a phosphoinositide-3-kinase (PI3K) inhibitor], PD98059 [a MAP/ERK 1 kinase (MEK1) inhibitor], CHIR99021 (a GSK-3b inhibitor), and BCAA significantly inhibited visfatin-induced proliferation in HepG2 cells. BCAA also inhibited phosphorylation of GSK-3b, increased cellular levels of p21 CIP1 , caused cell-cycle arrest in G 0 /G 1 phase, and induced apoptosis in HCC cells in the presence of visfatin. These findings suggest that visfatin plays a critical role in the proliferation of HCC cells and may be associated with the progression of this malignancy. In addition, BCAA might inhibit obesity-related liver carcinogenesis by targeting and, possibly, by overcoming the stimulatory effects of visfatin.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Possible Role of Visfatin in Hepatoma Progression and the Effects of Branched-Chain Amino Acids on Visfatin-Induced Proliferation in Human Hepatoma Cells

Ninomiya

Shimizu

Imai

et al. 2011

Cancer Prevention Research

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“…Taken together, our findings suggest that Nampt has an important role in regulating initiation and metastasis of gastric cancer. Nampt overexpression is known to contribute to tumor cell survival and proliferation in prostate cancer (8,24). This indicates that the blockade of the Namptstimulated signal pathway by this specific Nampt inhibitor may have therapeutic implications for the treatment of gastric cancer in which Nampt is overexpressed.…”

Section: Discussionmentioning

confidence: 98%

Overexpression of Nampt in gastric cancer and chemopotentiating effects of the Nampt inhibitor FK866 in combination with fluorouracil

Che

Liao³

et al. 2011

Oncol Rep

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Abstract. Nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in the NAD + salvage pathway, is overexpressed and important in the carcinogenesis in several types of cancers. The expression of Nampt and its role in gastric cancer remain largely unknown. In this study, using real-time PCR and Western blotting we found that Nampt was overexpressed at the mRNA and protein levels, respectively, in established gastric cancer cells and human gastric cancer tissues. The specific Nampt inhibitor FK866 repressed gastric cancer cell proliferation, as assessed by MTT assay. Using transwell and soft agar clonogenic assays, we also found that FK866 suppressed gastric cancer cell migration and anchorageindependent growth, respectively. These inhibitory effects of FK866 were accompanied by significantly decreased expression of VEGF, MMP2, MMP9 and NF-κB. As determined by MTT assay and flow cytometry, FK866 also increased the chemosensitivity of gastric cancer cells to fluorouracil by greater inhibition of cell proliferation and the induction of apoptosis. Our findings indicate that Nampt may be a new therapeutic target for gastric cancer. IntroductionGastric cancer is the fourth most common malignancy in the world and causes ~800,000 deaths annually worldwide (1). For patients with recurrent, metastatic, or advanced gastric cancer, fluorouracil (5-FU) is a commonly used chemotherapeutic drug (2). However, the toxic side effects associated with 5-FU remain a significant challenge to its use. The development of more effective therapeutic drugs with minimal side effects is crucial, and is dependent on a better understanding of the molecular mechanism underlying gastric carcinogenesis.Nicotinamide adenine dinucleotide (NAD) is an essential cofactor found in all cells and plays key roles as a carrier of electrons during redox reactions. The rate-limiting enzyme involved in the biosynthesis of NAD from the nicotinamide precursor is nicotinamide phosphoribosyltransferase (Nampt) (3). Increasing evidence demonstrates that Nampt is a multifunctional enzyme and is important in metabolism and immune response as well as cancer (4). Nampt is also known as pre-B-cell colony enhancing factor (PBEF1), a presumptive cytokine (5), and as visfatin, an insulin-mimetic adipocytokine secreted by visceral fat (6) that is also encoded by the PBEF1 gene (5).Cross-talk between the two NAD-dependent enzymes SIRT1 (also known as sirtuin 1 or NAD-dependent deacetylase sirtuins-1) deacetylase and poly(ADP-ribose) polymerase 1 (PARP1) plays a major role in cell viability under stress (7). By binding to and thereby causing the deacetylation of PARP1, SIRT1 protects cells from PARP1-mediated cell death. SIRT1 has also been shown to control PARP1 at the transcriptional level by negatively regulating the PARP1 gene promoter. The activity of SIRT1 can be positively regulated by Nampt, making Nampt a player in promoting cell survival under stress (8).Nampt was first reported to be overexpressed in colorectal cancer (9,10). It is also overexpressed i...

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“…In prostate carcinogenesis, NAMPT increased PC3 cell proliferation activating the mitogen-activated protein kinases (MAPKs) ERK-1/ERK-2 and p38 signaling pathways (Patel et al, 2010). NAMPT promoted the activity and expression of MMP-2/MMP-9 which represent important proteases involved in the breakdown of the extracellular matrix, indicating a possible role for NAMPT in PC metastasis (Patel et al, 2010).…”

Section: Oncogenesismentioning

confidence: 99%

NAMPT (nicotinamide phosphoribosyltransferase)

Koumaki¹,

Dalamaga²

2012

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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A novel role for the adipokine visfatin/pre-B cell colony-enhancing factor 1 in prostate carcinogenesis

Cited by 83 publications

References 27 publications

Possible Role of Visfatin in Hepatoma Progression and the Effects of Branched-Chain Amino Acids on Visfatin-Induced Proliferation in Human Hepatoma Cells

Possible Role of Visfatin in Hepatoma Progression and the Effects of Branched-Chain Amino Acids on Visfatin-Induced Proliferation in Human Hepatoma Cells

Overexpression of Nampt in gastric cancer and chemopotentiating effects of the Nampt inhibitor FK866 in combination with fluorouracil

NAMPT (nicotinamide phosphoribosyltransferase)

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