Visfatin triggers the in vitro migration of osteosarcoma cells via activation of NF-κB/IL-6 signals

Wang, Guangji; Shen, Ningjiang; Cheng, Liang; Fang, Yehan; Huang, Haohai; Li, Kanghua

doi:10.1016/j.ejphar.2016.08.029

Cited by 22 publications

(20 citation statements)

References 34 publications

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“…The underlying mechanisms by which IL‐37 inhibits IL‐6 expression in NSCLC also remain unclear. NF‐kB has been reported to be a critical regulator of many genes regulating tumor progression and could mediate IL‐6 secretion in cancer . Further studies are needed to establish the mechanisms underlying the anti‐tumor activity of IL‐37 in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

IL‐37 inhibits invasion and metastasis in non‐small cell lung cancer by suppressing the IL‐6/STAT3 signaling pathway

et al. 2018

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BackgroundIL‐37 has been identified as a fundamental inhibitor of inflammatory and immunity responses. It plays a crucial protective role in several cancers, but its anti‐tumor activity and the potential regulatory mechanism of IL‐37 in non‐small cell lung cancer (NSCLC) is largely unclear.MethodsEnzyme‐linked immunosorbent assay was used to detect plasma IL‐37 expression in NSCLC patients and healthy controls. The NSCLC cell line A549 was cultured with recombinant human IL‐37 or recombinant human IL‐6 protein. A549 invasion and metastasis were detected using Transwell invasion and scratch wound healing assays, respectively. Protein expression of STAT3, pSTAT3, E‐cadherin, vimentin, and N‐cadherin were detected using Western blotting, and messenger RNA expression of STAT3, E‐cadherin, vimentin, and N‐cadherin was assessed in each group using real time PCR.ResultsIL‐37 plasma expression was decreased in NSCLC patients, and the downregulation of IL‐37 was correlated with tumor stage. In vitro, IL‐37 inhibited invasion and migration in A549 cells, while IL‐6 promoted invasion and migration in A549 cells. pSTAT3, vimentin, and N‐cadherin expression was increased. E‐cadherin expression was lower in the IL‐6 group than in the control group; however, the opposite pattern was observed in the IL‐37 + IL‐6 group.ConclusionOur results showed that IL‐37 plays an inhibitory role in NSCLC progression, possibly by suppressing STAT3 activation and decreasing epithelial‐to‐mesenchymal transition by inhibiting IL‐6 expression. IL‐37 could serve as a potential novel tumor suppressor in NSCLC.

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Section: Discussionmentioning

confidence: 99%

IL‐37 inhibits invasion and metastasis in non‐small cell lung cancer by suppressing the IL‐6/STAT3 signaling pathway

et al. 2018

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“…Recently, some studies have indicated that NAMPT acts as a regulator of cancer invasion and metastasis [5,39,40], which is one of the hallmarks of malignant cancer cells [41]. However, the current understanding of the role that NAMPT plays in invasion and metastasis remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…However, the current understanding of the role that NAMPT plays in invasion and metastasis remains unclear. The overexpression of NAMPT could significantly enhance the abilities of invasion and migration in osteosarcoma and glioma cells [5,39,40]; however, some studies draw the opposite conclusion that the knockdown of NAMPT promotes metastatic aggressiveness in breast cancer cells [42]. Intriguingly, NAMPTinduced epithelial-to-mesenchymal transition has been shown to be modulated by secreted NAMPT and to be independent of FK866 and of NAD + intermediate treatment [43].…”

Section: Discussionmentioning

confidence: 99%

“…Intriguingly, NAMPTinduced epithelial-to-mesenchymal transition has been shown to be modulated by secreted NAMPT and to be independent of FK866 and of NAD + intermediate treatment [43]. Therefore, the positive correlation between NAMPT overexpression and the migration capacity in some studies might be due to the increased secretion of NAMPT [39]. Our results indicate that the knockdown of NAMPT failed to impair the tendency of invasion and migration in both HCT116 and LoVo cells, but we do not know whether the overexpression of NAMPT in this setting would influence the migration ability.…”

Section: Discussionmentioning

confidence: 99%

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Targeting the NAD+ salvage pathway suppresses APC mutation-driven colorectal cancer growth and Wnt/β-catenin signaling via increasing Axin level

et al. 2020

Cell Commun Signal

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Background: The role and mechanism of the nicotinamide adenine dinucleotide (NAD +) salvage pathway in cancer cell proliferation is poorly understood. Nicotinamide phosphoribosyltransferase (NAMPT), which converts nicotinamide into NAD + , is the rate-limiting enzyme in the NAD + salvage pathway. Here, we assessed the role of NAMPT in the proliferation of colorectal cancer. Methods: Real-time PCR, immunohistochemistry, western blotting, and analyses of datasets from Oncomine and Gene Expression Omnibus were conducted to assess the expression of NAMPT at the mRNA and protein levels in colorectal cancer. The Kaplan Meier plotter online tool was used to evaluate the prognostic role of NAMPT. Knockdown of NAMPT was performed to assess the role of NAMPT in colorectal cancer cell proliferation and tumorigenesis both in vitro and in vivo. Overexpression of NAMPT was used to evaluate impact of NAMPT on colorectal cancer cell proliferation in vitro. NAD + quantitation, immunofluorescence, dual luciferase assay and western blot were used to explore the mechanism of colorectal cancer proliferation. Transwell migration and invasion assays were conducted to assess the role of NAMPT in cell migration and invasion abilities of colorectal cancer cells. Results: Our study indicated that the inhibition of NAMPT decreased proliferation capacity of colorectal cancer cells both in vitro and in vivo. Conversely, overexpression of NAMPT could promote cell proliferation in vitro. NAMPT inhibition induced β-catenin degradation by increasing Axin expression levels; this resulted in the inhibition of Wnt/ β-catenin signaling and cell proliferation in colorectal cancer. The addition of nicotinamide mononucleotide, the enzymatic product of NAMPT, effectively reversed β-catenin protein degradation and inhibited growth. Similarly, the knockdown of Axin also decreased the cell death induced by the inhibition of NAMPT. In addition, we showed that colorectal cancer tissues harbored significantly higher levels of NAMPT than the levels harbored by paired normal tissues, especially in colorectal cancer stages I and II. And the overexpression of NAMPT was associated with unfavorable survival results.

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“…Accumulated evidence indicated that NAMPT serves signi cant effects in different types of cancer and inhibition of NAMPT may be used as a therapeutic method in cancer (6)(7)(8). Moreover, Wang et al (9) indicated that NAMPT promotes the migration of OS cells in vitro by activating NF-κB/IL-6 signals. Previous studies by our research team have shown that NAMPT serves signi cant effects on epithelial-mesenchymal transition, migration and invasion of OS cells (10).…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells

Gong

Huang

Cao

et al. 2020

Preprint

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Background: Visfatin is a novel adipokine, also known as a nicotinamide phosphorybosyltransferase (NAMPT) that is reported to promote the progression of osteosarcoma. The research sought to determine the regulatory network underlying NAMPT on osteosarcoma (OS).Method: The OS tissues and paired normal controls were collected from 45 OS patients. The binding relationship between microRNA-26a-5p (miR-26a-5p) and two genes (NAMPT and NORAD) were predicted by TargetScan V7.2 and confirmed by dual-luciferase reporter assay. To reveal the function of long noncoding RNA NORAD/miR-26a-5p/NAMPT axis on cell viability, cell cycle and apoptosis of U2OS cells, CCK-8 and flow cytometry assays, examination of apoptosis-associated molecules (Bcl-2, Bax, cleaved (C)-caspase-3) were performed. The mRNA and protein levels were separately examined by RT-qPCR and Western blot. Results: NAMPT and NORAD expressions were increased in OS tissue samples, while miR-26a-5p expression was decreased. Functionally, NORAD functions as a ceRNA of miR-136-5p to competitively target NAMPT. Furthermore, miR-26a-5p overexpression inhibited viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating NAMPT along with change the expressions of apoptosis-related molecules. NORAD overexpression promoted viability, cell cycle and apoptosis resistance of U2OS cells by down-regulating MiR-26a-5p along with changes of the expressions of apoptosis-related molecules.Conclusion: LncRNA NORAD, serving as a ceRNA of miR-26a-5p, promoted proliferation and apoptosis resistance of U2OS cells by upregulation of NAMPT.

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Visfatin triggers the in vitro migration of osteosarcoma cells via activation of NF-κB/IL-6 signals

Cited by 22 publications

References 34 publications

IL‐37 inhibits invasion and metastasis in non‐small cell lung cancer by suppressing the IL‐6/STAT3 signaling pathway

IL‐37 inhibits invasion and metastasis in non‐small cell lung cancer by suppressing the IL‐6/STAT3 signaling pathway

Targeting the NAD+ salvage pathway suppresses APC mutation-driven colorectal cancer growth and Wnt/β-catenin signaling via increasing Axin level

Long Noncoding RNA NORAD/MiR-26a-5p/NAMPT (Visfatin) Axis Regulates Proliferation and Apoptosis of Human Osteosarcoma Cells

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