Types of human malignant tumors, including liver, colon, ovarian,įurthermore, YAP has been associated with tumor development and the Consistently, upregulated YAPĮxpression and nuclear localization have been observed in multiple Gene locus is amplified in human malignancies, including glioma,Ĭell carcinoma and hepatocellular carcinoma (HCC) ( 21). Regulates multiple cellular processes and is associated with tumor Yes-associated protein (YAP), a transcriptionalĬo-activator that acts downstream of the Hippo signaling pathway, Elevated Sirt1 deacetylates activatedĭamaged DNA to proliferate, promoting tumor development ( 18). ( 14), breast ( 15) and gastric cancer ( 16). The growth, metastasis and chemotherapy resistance of a number ofĬancers through its anti-apoptotic activity, including colon Its targets in specific signaling pathways or the specific type ofĭemonstrated that Sirt1 is involved in carcinogenesis and enhances Remains unclear, since it seems to depend on the cellular context, Whether Sir1 serves a role as a tumor suppressor or tumor promoter Role of Sirt1 in cancers has been studied previously however, Regulatory molecules, including tumor protein p53 ( 12, 13). Including DNA repair, metabolism and cell survival under genotoxicįunctions as a NAD +-dependent histone deacetylase, andĭeacetylates a number of key cell cycle proteins and apoptosis Silent mating-type information regulation 2 homologġ (Sirt1), originally identified as a longevity gene, is induced byĬaloric restriction and regulates various cellular functions, Was demonstrated to be upregulated in numerous types of human Visfatin acts as a NADīiosynthetic enzyme similar to nicotinamide phosphoribosylĪs an enzyme involved in the NAD + salvage pathway, which Prove to be an important mechanistic link in the network of factorsĪffecting obesity-associated tumor growth. Individuals and contributes to a general pro-inflammatory state in The level of one such adipokine, visfatin, increases in obese The most abundant adipokines derived fromĪdipose tissue have been implicated as mediators of the effects of Obesity affects cancer growth are currently being investigated Īdipokine, hormonal, inflammatory and immunological changes mayĬontribute in part to altered tumor biology ( 5). Of gastric cancer through complex molecular mechanisms, which Numerous types of cancer including colorectal, postmenopausalīreast, prostate and renal cancer ( 3), and esophageal and gastric adenocarcinoma Obesity, a worldwide epidemic ( 2), is associated with an increased risk of Identify the potential of novel targets for therapeutic Underlying molecular mechanisms of gastric cancer growth and Malignant tumor and the third leading cause of cancer-associatedĪggressiveness of gastric cancer biology and the limitedĮffectiveness of current therapeutic modalities with advancedĭisorders, further studies are required in order to understand the Gastric cancer is the fifth most common form of These results suggested that diet‑induced obesity could promote murine gastric cancer growth by modulating the Sirt1/YAP signaling pathway. In addition, a positive correlation was observed between Sirt1 expression and YAP expression, and between Sirt1 expression and serum visfatin levels in mice. Murine forestomach carcinoma (MFC) cells treated with 5% sera from obese mice exhibited significantly increased expression of Sirt1 and YAP compared with MFC cells treated with sera from lean mice. In addition, markedly increased levels of Sirt1 and YAP protein were observed in the nucleus of cells from subcutaneous tumors from obese mice compared with those from lean mice. In a subcutaneous mouse model, tumors were significantly larger in obese mice compared with non‑obese and lean mice. The aim of the present study was to investigate the potential molecular mechanisms through which obesity affects gastric cancer growth. However, the molecular mechanisms underlying this association remain unclear and require further investigation. A previous study from our group using an in vivo model demonstrated that diet induced‑obesity increases the risk of gastric cancer and may prompt its growth.
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