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Liu P.,Shandong University | Kong F.,Shandong University | Wang J.,Shandong University | Lu Q.,Shandong University | And 3 more authors.
Experimental Cell Research | Year: 2015

Perivascular adipocyte (PVAC) proliferation and differentiation were closely involved in cardiovascular disease. We aimed to investigate whether phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways enhance PVAC functions activated by insulin-like growth factor 1(IGF-1) and suppressed by mesenchyme homeobox 2 (MEOX2). In this study, PVACs from primary culture were cultured and induced to differentiate. Cell viability assays demonstrated that IGF-1 promoted PVAC proliferation and differentiation. However MEOX2 counteracted these IGF-1-mediated actions. Flow Cytometry revealed that IGF-1 increased S phase cells and decreased apoptosis; however, MEOX2 decreased S phase cells, increased G0-G1 phase cells, and promoted apoptosis. During PVAC proliferation and differentiation, IGF-1 activated PI3K/Akt1/2 and ERK1/2 signaling pathways, upregulated the expression of these signaling proteins and FAS, and increased PVAC lipid content. In contrast, MEOX2 constrained the phosphorylation of ERK1/2 and Akt1/2 protein, down-regulated these signaling molecules and FAS, and decreased PVAC lipid content. Instead, MEOX2 knockdown enhanced the ERK1/2 and Akt1/2 phosphorylation, augmented the expression of these signaling molecules and FAS, and increased PVAC lipid content. Our findings suggested that PI3K/Akt1/2 and ERK1/2 activation mediated by IGF-1 is essential for PVAC proliferation and differentiation, and MEOX2 is a promising therapeutic gene to intervene in the signaling pathways and inhibit PVAC functions. © 2014 Elsevier Inc.

Zhu S.,Wendeng Central Hospital of Weihai City | Shao B.,Wendeng Central Hospital of Weihai City | Hao Y.,General Hospital of Peoples Liboration Army | Li Z.,Wendeng Central Hospital of Weihai City | And 4 more authors.
Cancer Biomarkers | Year: 2015

BACKGROUND: Ghrelin was associated with several of cancers. The conflict results of SNPs with GHRL and GHSR gene were demonstrated in different studies. Thus, this meta-analysis is to evaluate the associations.METHODS: Systematic literature search was done on PubMed database up to October 2013. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association by a fixed-effect model and a random-effect model.RESULTS: A total of 7 studies, which included 3 studies for breast cancer, 2 for colorectal cancer, 1 for hepatocellular carcinoma, 1 for esophageal cancer and 1 for Non-Hodgkin lymphoma. When analyzed all the GHRL SNPs with all kinds of cancers, there was significantly difference with cancer patients compared with controls (Recessive model: OR 0.938, 95% CI 0.890-0.989, p=0.017), while no significant difference was existed in the additive model (OR 0.9903, 95% CI 0.957-1.024, p=0.558) and dominant model (OR 1.014, 95% CI 0.970-1.061, p=0.536). When analyzed all the GHSR SNPs with all kinds of cancers, no significant difference was observed.CONCLUSION: Our results suggest that the SNP with GHRL and GHSR might be weaker association with cancer risk, especially with breast cancer risk. © 2015 - IOS Press and the authors. All rights reserved.

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