Secretion of One Adipokine Nampt/Visfatin Suppresses the Inflammatory Stress‐Induced NF‐<i>κ</i>B Activity and Affects Nampt‐Dependent Cell Viability in Huh‐7 Cells

Lin, Yi; Wu, Hui Chung; Liao, Chen Chung; Chou, Yi Chih; Pan, Shwu Fen; Chiu, Chi Ming

doi:10.1155/2015/392471

Cited by 15 publications

(9 citation statements)

References 36 publications

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“…Our study has a few limitations. Visfatin, as a form of extracellular NAMPT, is susceptible to overexpression under oxidative stress in HCC cells; it then inhibits the growth of hepatoma cells [ 34 ]. In contrast, Buldak et al [ 30 ] observed that elevated visfatin levels induced antioxidant capacity and promoted melanoma cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Elevated serum visfatin levels are associated with poor prognosis of hepatocellular carcinoma

Sun

Zhu

et al. 2017

Oncotarget

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Visfatin is considered a pro-inflammatory adipocytokine, and it is commonly increased in obesity-related diseases. This study aimed to evaluate the levels of serum visfatin in patients with hepatocellular carcinoma (HCC) and its diagnostic and predictive value in detecting HCC. Fasting serum levels of visfatin of 135 HCC patients, 115 chronic hepatitis B (CHB) patients, 129 liver cirrhosis (LC) patients, and 149 healthy controls were determined via enzyme-linked immunosorbent assay. Meanwhile, serum alpha fetal protein (AFP) and interleukin-6 (IL-6) were also assayed. The median serum visfatin concentration in HCC patients was 1.113 ng/ mL (range: 0.823-2.214 ng/mL), which was significant higher than those of healthy controls, CHB patients, and LC patients (P<0.05). The serum visfatin concentration in HCC patients was positively correlated with AFP (r=0.595, P<0.001) and IL-6 (r=0.261, P<0.015) and was also associated with tumor size and tumor node metastasis stage. Moreover, elevated levels of serum visfatin were associated with a higher HCC risk for CHB and LC patients. Multivariate Cox regression analysis had shown that HCC patients with high levels of serum visfatin had significantly shorter overall survival times than those with low serum visfatin levels (P<0.001). Using a cutoff visfatin level of 1.403 ng/mL, the receiver operating characteristic curve analysis showed unappealing sensitivity and specificity values (45.76% and 74.79%, respectively; AUC=0.626) regarding visfatin's use as a diagnostic marker for HCC. Our results indicate that increased serum visfatin levels are associated with poor prognosis of HCC. Visfatin may be a potential therapeutic target of HCC.

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Section: Discussionmentioning

confidence: 99%

Elevated serum visfatin levels are associated with poor prognosis of hepatocellular carcinoma

Sun

Zhu

et al. 2017

Oncotarget

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“…Firstly, AMPK is a key sensor of ATP resources in the cell, and is essential for rhythmicity of NAMPT in WAT. Furthermore, the ratio NAD+/NADH determines the production of reactive oxygen species (ROS), and oxidative stress increases NAMPT release (Lin et al 2015;Lu et al 2019). Consequently, NAMPT inhibition induces susceptibility to oxidative stress (Hong et al 2016;Xu et al 2017).…”

Section: Nampt Retains More Rhythmicity Than the Core Clock After Scn Lesionsmentioning

confidence: 99%

Thermal lesions of the SCN do not abolish all gene expression rhythms in rat white adipose tissue, NAMPT remains rhythmic

Spek

Foppen

Fliers

et al. 2021

Chronobiology International

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Obesity and type 2 diabetes mellitus are major health concerns worldwide. In obese-type 2 diabetic patients, the function of the central brain clock in the hypothalamus, as well as rhythmicity in white adipose tissue (WAT), are reduced. To better understand how peripheral clocks in white adipose tissue (WAT) are synchronized, we assessed the importance of the central brain clock for daily WAT rhythms. We compared gene expression rhythms of core clock genes (Bmal1, Per2, Cry1, Cry2, RevErbα, and DBP) and metabolic genes (SREBP1c, PPARα, PPARγ, FAS, LPL, HSL, CPT1b, Glut4, leptin, adiponectin, visfatin/NAMPT, and resistin) in epididymal and subcutaneous white adipose tissue (eWAT and sWAT) of SCN-lesioned and sham-lesioned rats housed in regular L/D conditions. Despite complete behavioral and hormonal arrhythmicity, SCN lesioning only abolished Cry2 and DBP rhythmicity in WAT, whereas the other clock gene rhythms were significantly reduced, but not completely abolished. We observed no major differences in the effect of SCN lesions between the two WAT depots. In contrast to clock genes, all metabolic genes lost their daily rhythmicity in WAT, with the exception of NAMPT. Interestingly, NAMPT rhythmicity was even less affected by SCN lesioning than the core clock genes, suggesting that it is either strongly coupled to the remaining rhythmicity in clock gene expression, or very sensitive to other external rhythmic factors. The L/D cycle could be such a rhythmic external factor that generates modulating signals by photic masking via the intrinsic photosensitive retinal ganglion cells in combination with the autonomic nervous system. Our findings indicate that in normal weight rats, gene expression rhythms in WAT can be maintained independent of the central brain clock.

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“…Indeed, this hypothesis is strengthened by observations that similar stress conditions, including ischaemia (Jing et al , ) and oxygen–glucose deprivation (OGD), strongly increase eNAMPT release in neurons and glial cells (Zhao et al , ) as well as hypoxia in melanoma cells (Grolla et al , ). Similarly, oxidative and endoplasmic reticulum (ER) stress also appear to increase eNAMPT release (Huh‐7 cells) (Pillai et al , ; Lin et al , ). These observations also remain to be systematically investigated.…”

Section: Introductionmentioning

confidence: 99%

Extracellular nicotinamide phosphoribosyltransferase, a new cancer metabokine

Grolla

Travelli

Genazzani

et al. 2016

British J Pharmacology

107

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In this review, we focus on the secreted form of nicotinamide phosphoribosyltransferase (NAMPT); extracellular NAMPT (eNAMPT), also known as pre‐B cell colony‐enhancing factor or visfatin. Although intracellular NAMPT is a key enzyme in controlling NAD metabolism, eNAMPT has been reported to function as a cytokine, with many roles in physiology and pathology. Circulating eNAMPT has been associated with several metabolic and inflammatory disorders, including cancer. Because cytokines produced in the tumour micro‐environment play an important role in cancer pathogenesis, in part by reprogramming cellular metabolism, future improvements in cancer immunotherapy will require a better understanding of the crosstalk between cytokine action and tumour biology. In this review, the knowledge of eNAMPT in cancer will be discussed, focusing on its immunometabolic function as a metabokine, its secretion, its mechanism of action and possible roles in the cancer micro‐environment.

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Secretion of One Adipokine Nampt/Visfatin Suppresses the Inflammatory Stress‐Induced NF‐κB Activity and Affects Nampt‐Dependent Cell Viability in Huh‐7 Cells

Cited by 15 publications

References 36 publications

Elevated serum visfatin levels are associated with poor prognosis of hepatocellular carcinoma

Elevated serum visfatin levels are associated with poor prognosis of hepatocellular carcinoma

Thermal lesions of the SCN do not abolish all gene expression rhythms in rat white adipose tissue, NAMPT remains rhythmic

Extracellular nicotinamide phosphoribosyltransferase, a new cancer metabokine

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