Visfatin increases miR-21 to promote migration in HCC

Liang, Ning-Lin; Chen, Yongjun; Yang, Li; He, Suyu; Li, Tianyu

doi:10.14715/cmb/2018.64.6.9

Cited by 13 publications

(13 citation statements)

References 40 publications

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“…Our data also show a significant increase in the serum levels of visfatin in HCC and HCV patients compared to the NC groups. These data are in concordance with these of Ninomiya et al, (2011) and Liang et al, (2018) who found that visfatin level is significantly higher in HCC patients compared to control group, and that it induces HCC cell migration via upregulation of miR-21. In our study, we found that increased serum level of visfatin associates significantly with increased mortality rates of the patients.…”

Section: Discussionsupporting

confidence: 92%

The Possible Role of Adipokines in HCV Associated Hepatocellular Carcinoma

Eldaly

Saber

Abdellateif

et al. 2020

Asian Pac J Cancer Prev

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Background: Adipokines play an important role in the regulation of inflammation and tumor progression. Aim: Assessment of the possible role of adiponectin, leptin and visfatin in HCV associated hepatocellular carcinoma (HCC). Methods: patients were classified into 85 patients with HCV associated HCC, 100 patients with chronic hepatitis C viral (HCV) infection compared to 50 normal control (NC) subjects. All subjects included in the study were assessed for HCV infection by seropositive HCV antibodies, as well as HCV RNA by RT-PCR. Serum levels of adiponectin, leptin and visfatin were assessed using enzyme linked immunosorbent assay (ELISA). The data were correlated to the relevant clinic-pathological features of the patients, and the overall survival (OS) rate. Results: There was a significant difference in the serum levels of adiponectin and visfatin among HCC, HCV and NC groups (P<0.001). The serum levels of leptin and alpha fetoprotein (AFP) were significantly higher in HCC group (P<0.001). There was a significant association between the serum level of adiponectin and advanced Child class liver cirrhosis (P=0.03), as well as with poor performance status (ECOG, P=0.02). Serum leptin associated significantly with the number of lesions in the liver (P=0.006), visfatin associated with increased mortality rate (P<0.001). Adiponectin, leptin and visfatin associated significantly with liver cirrhosis in HCV patients (P<0.01). Leptin achieved the highest sensitivity (98.8%). visfatin achieved the highest specificity (100%) and PPV (100%) for detection of HCC. The combination of serum leptin and visfatin for the diagnosis of HCV associated HCC showed sensitivity, specificity, PPV, NPV and accuracy (100%, 96.6%, 93.4%, 100% and 97.4%; respectively). Conclusion: Adiponectin, leptin and visfatin have an important role(s) in the pathogenesis of HCV associated HCC.

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Section: Discussionsupporting

confidence: 92%

The Possible Role of Adipokines in HCV Associated Hepatocellular Carcinoma

Eldaly

Saber

Abdellateif

et al. 2020

Asian Pac J Cancer Prev

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“…Experimental evidence shows that mi RNAs can be used as oncogenes or tumor suppressor genes in HCC [36]. For example, miR-21 is used as a cancer-promoting factor in HCC, which is highly expressed in HCC and induces cell proliferation, invasion and chemotherapy resistance [37]. In contrast, miR-122, as a tumor suppressor, is lowly expressed in HCC [38].…”

Section: Discussionmentioning

confidence: 99%

Lnc-RNA CASC15 promotes HCC progression via modulation of Six1 targeted by miR-2355-5p

Han

Sui

Tao

et al. 2020

Preprint

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Background: Long-chain non-coding RNA (LncRNA) plays a key role in the biological processes of tumors. LncRNA CASC15 has been shown to be involved in the development of a variety of tumors. The study aimed to elucidate the mechanism of lncRNA CASC15 in the progression of hepatocellular carcinomas (HCC). Methods: qRT-PCR was used to detect the expression levels of CASC15, miR-2355-5p and Six1 mRNA in HCC tissues and cells. Six1 protein expression levels were detected by Western Blot. CCK-8 experiment, colony formation experiment, Edu staining and Transwell experiment analysis were used to analyze the effects of CASC15, miR-2355-5p and Six1 on cell proliferation, cell invasion and migration. The relationship between CASC15, miR-2355-5p and Six1 was analyzed using bioinformatics analysis and Luciferase. Result: CASC15 was raised in HCC tissues and HCC cells. Down-regulation of CASC15 inhibited the growth, migration, invasion and tumor growth of HCC cells. The expression level of miR-2355-5p was reduced in HCC tissues. In addition, miR-2355-5p inhibitor induced the growth, migration and invasion of HCC cells. MiR-2355-5p was predicted to be a downstream target of CASC15. The expression level of miR-2355-5p was negatively correlated with CASC15 in HCC tumor tissues. Six1 was predicted to be a downstream target of miR-30a-5p. In vitro and in vivo results showed that CASC15/miR-2355-5p can regulate Six1.Conclusion: LncCASC15 regulated the proliferation and invasion of Six1 by binding with miR-2355-5p in HCC, suggesting that CASC15 may be a potential target for HCC.

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“…NAMPT is a pleiotropic protein implicated in the pathogenesis of cancer and obesity and its complications, including insulin resistance, diabetes, and aging (Goktas et al 2013;Shackelford et al 2013;Zhang et al 2017;Zhao et al 2017;Liang et al 2018;Poljsak 2018;Ohanna et al 2018). There are data reporting that inhibition of NAMPT by specific inhibitors decreases cancer growth, induces apoptosis, suppresses cell growth, and enhances the susceptibility to oxidative stress and also sensitizes the glioblastoma cells to temozolomide (Abu Aboud et al 2016;Feng et al 2016;Alaee et al 2017;Xu et al 2017;Tabassum et al 2018).…”

mentioning

confidence: 99%

“…It has also been shown that down-regulation of NAMPT expression by miR-206 reduces survival of the breast cancer cells that NAMPT expression is up-regulated in pediatric gliomas and that its overexpression induces glioma and other cancers growth (Minchenko et al 2015a;Lucena-Cacace et al 2017;Zhao et al 2017;Hesari et al 2018). Moreover, NAMPT can promote hepatocellular carcinoma cell migration through the up-regulation of miR-21 (Liang et al 2018).…”

mentioning

confidence: 99%

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Silencing of NAMPT leads to up-regulation of insulin receptor substrate 1 gene expression in U87 glioma cells

Tsymbal

Minchenko

Luzina

et al. 2020

Endocrine Regulations

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Objective. The aim of the present study was to investigate the effect of adipokine NAMPT (nicotinamide phosphoribosyltransferase) silencing on the expression of genes encoding IRS1 (insulin receptor substrate 1) and some other proliferation related proteins in U87 glioma cells for evaluation of the possible significance of this adipokine in intergenic interactions.Methods. The silencing of NAMPT mRNA was introduced by NAMPT specific siRNA. The expression level of NAMPT, IGFBP3, IRS1, HK2, PER2, CLU, BNIP3, TPD52, GADD45A, and MKI67 genes was studied in U87 glioma cells by quantitative polymerase chain reaction. Anti-visfatin antibody was used for detection of NAMPT protein by Western-blot analysis.Results. It was shown that the silencing of NAMPT mRNA led to a strong down-regulation of NAMPT protein and significant modification of the expression of IRS1, IGFBP3, CLU, HK2, BNIP3, and MKI67 genes in glioma cells and a strong up-regulation of IGFBP3 and IRS1 and down-regulation of CLU, BNIP3, HK2, and MKI67 gene expressions. At the same time, no significant changes were detected in the expression of GADD45A, PER2, and TPD52 genes in glioma cells treated by siRNA specific to NAMPT. Furthermore, the silencing of NAMPT mRNA suppressed the glioma cell proliferation.Conclusions. Results of this investigation demonstrated that silencing of NAMPT mRNA with corresponding down-regulation of NAMPT protein and suppression of the glioma cell proliferation affected the expression of IRS1 gene as well as many other genes encoding the proliferation related proteins. It is possible that dysregulation of most of the studied genes in glioma cells after silencing of NAMPT is reflected by a complex of intergenic interactions and that NAMPT is an important factor for genome stability and regulatory mechanisms contributing to the control of glioma cell metabolism and proliferation.

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Visfatin increases miR-21 to promote migration in HCC

Cited by 13 publications

References 40 publications

The Possible Role of Adipokines in HCV Associated Hepatocellular Carcinoma

The Possible Role of Adipokines in HCV Associated Hepatocellular Carcinoma

Lnc-RNA CASC15 promotes HCC progression via modulation of Six1 targeted by miR-2355-5p

Silencing of NAMPT leads to up-regulation of insulin receptor substrate 1 gene expression in U87 glioma cells

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