Obesity and cancer: the role of adipose tissue and adipo-cytokines-induced chronic inflammation

被引:276
作者
Divella, Rosa [1 ]
De Luca, Raffaele [2 ]
Abbate, Ines [1 ]
Naglieri, Emanuele [3 ]
Daniele, Antonella [1 ]
机构
[1] Giovanni Paolo II Natl Canc Inst, Dept Expt Oncol, Clin Pathol Lab, V Le Orazio Flacco 65, I-70124 Bari, Italy
[2] Giovanni Paolo II Natl Canc Inst, Dept Surg Oncol, V Le Orazio Flacco 65, I-70124 Bari, Italy
[3] Giovanni Paolo II Natl Canc Inst, Dept Med Oncol, V Le Orazio Flacco 65, I-70124 Bari, Italy
关键词
adipocytes inflammation; adipocytokine; obesity; cancer; TUMOR-NECROSIS-FACTOR; BODY-MASS INDEX; SQUAMOUS-CELL CARCINOMA; NITRIC-OXIDE SYNTHASE; DIET-INDUCED OBESITY; INDUCIBLE FACTOR-I; BREAST-CANCER; INSULIN-RESISTANCE; TNF-ALPHA; OXIDATIVE STRESS;
D O I
10.7150/jca.16884
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Adipose tissue in addition to its ability to keep lipids is now recognized as a real organ with both metabolic and endocrine functions. Recent studies demonstrated that in obese animals is established a status of adipocyte hypoxia and in this hypoxic state interaction between adipocytes and stromal vascular cells contribute to tumor development and progression. In several tumors such as breast, colon, liver and prostate, obesity represents a poor predictor of clinical outcomes. Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro-inflammatory factors and a consequent alteration of key signaling mediators which may be an active local player in establishing the peritumoral environment promoting tumor growth and progression. Therefore, adipose tissue hypoxia might contribute to cancer risk in the obese population. To date the precise mechanisms behind this obesity-cancer link is not yet fully understood. In the light of information provided in this review that aims to identify the key mechanisms underlying the link between obesity and cancer we support that inflammatory state specific of obesity may be important in obesity-cancer link.
引用
收藏
页码:2346 / 2359
页数:14
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