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首页> 外文期刊>Cytokine >Stop feeding cancer: Pro-inflammatory role of visceral adiposity in liver cancer
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Stop feeding cancer: Pro-inflammatory role of visceral adiposity in liver cancer

机译：停止进食癌症：内脏肥胖在肝癌中的促炎作用

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Liver cancer is the fifth most common cancer in the world with an estimated over half a million new cases diagnosed every year. Due to the difficulty in early diagnosis and lack of treatment options, the prevalence of liver cancer continues to climb with a 5-year survival rate of between 6% and 11%. Coinciding with the rise of liver cancer, the prevalence of obesity has rapidly increased over the past two decades. Evidence from epidemiological studies demonstrates a higher risk of hepatocellular carcinoma (HCC) in obese individuals. Obesity is recognised as a low-grade inflammatory disease, this is of particular relevance as inflammation has been proposed as the seventh hallmark of cancer development with abdominal visceral adiposity considered as an important source of pro-inflammatory stimuli. Emerging evidence points towards the direct role of visceral adipose tissue rather than generalised body fat in carcinogenesis. Cytokines such as IL-6 and TNF-α secreted from visceral adipose tissue have been demonstrated to induce a chronic inflammatory condition predisposing the liver to a protumourigenic milieu. This review focuses on excess visceral adiposity rather than simple obesity; particularly adipokines and their implications for chronic inflammation, lipid accumulation, insulin resistance, Endoplasmic Reticulum (ER) stress and angiogenesis. Evidence of molecular signalling pathways that may give rise to the onset and progression of HCC in this context are depicted. Delineation of the pro-inflammatory role of visceral adiposity in liver cancer and its targeting will provide better rational and therapeutic approaches for HCC prevention and elimination. The concept of a central role for metabolism in cancer is the culmination of an effort that began with one of the 20th century's leading biochemists and Nobel laureate of 1931, Otto Warburg.
机译：肝癌是世界上第五大最常见的癌症，每年估计诊断出超过一百万的新病例。由于早期诊断的困难和缺乏治疗选择，肝癌的患病率持续上升，其5年生存率在6％至11％之间。伴随着肝癌的上升，在过去的二十年中，肥胖症的发病率迅速增加。流行病学研究的证据表明，肥胖个体患肝细胞癌（HCC）的风险更高。肥胖被认为是一种低度的炎症性疾病，与肥胖症特别相关，因为已提出炎症是癌症发展的第七个标志，而腹部内脏脂肪被认为是促炎性刺激的重要来源。越来越多的证据表明内脏脂肪组织直接作用而不是全身脂肪在致癌作用中的作用。从内脏脂肪组织分泌的细胞因子，例如IL-6和TNF-α已被证明可诱发慢性炎症，使肝脏容易患上致肿瘤的环境。本文的重点是内脏脂肪过多，而非单纯性肥胖。特别是脂肪因子及其对慢性炎症，脂质蓄积，胰岛素抵抗，内质网（ER）应激和血管生成的影响。描述了在这种情况下可能引起HCC的发生和发展的分子信号传导途径的证据。内脏脂肪在肝癌中的促炎作用及其靶向作用的描述将为预防和消除HCC提供更好的合理和治疗方法。癌症中新陈代谢的核心作用概念是一项努力的高潮，这项努力始于20世纪最著名的生物化学家之一和1931年的诺贝尔奖获得者奥托·沃堡。

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