Crosstalk between obesity and cancer: a role for adipokines.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-04-01 Epub Date: 2021-10-13 DOI:10.1080/13813455.2021.1988110

Zoya Tahergorabi, Hamed Lotfi, Maryam Rezaei, Mohammad Aftabi, Mitra Moodi

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Abstract

Adipose tissue is a complex organ that is increasingly being recognised as the largest endocrine organ in the body. Adipocytes among multiple cell types of adipose tissue can secrete a variety of adipokines, which are involved in signalling pathways and these can be changed by obesity and cancer. There are proposed mechanisms to link obesity/adiposity to cancer development including adipocytokine dysregulation. Among these adipokines, leptin acts through multiple pathways including the STAT3, MAPK, and PI3K pathways involved in cell growth. Adiponectin has the opposite action from leptin in tumour growth partly because of increased apoptotic responses of p53 and Bax. Visfatin increases cancer cell proliferation through ERK1/2, PI3K/AKT, and p38 which are stimulated by proinflammatory cytokines. Omentin through the PI3K/Akt-Nos pathway is involved in cancer-tumour development. Apelin might be involved through angiogenesis in tumour progressions. PAI-1 via its anti-fibrinolytic activity on cell adhesion and uPA/uPAR activity influence cancer cell growth.

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肥胖与癌症之间的相互影响：脂肪因子的作用。

脂肪组织是一个复杂的器官，越来越被认为是人体最大的内分泌器官。脂肪组织多种细胞类型中的脂肪细胞可分泌多种脂肪因子，这些因子参与信号通路，肥胖和癌症可改变这些信号通路。肥胖/肥胖与癌症发展之间的关联机制包括脂肪细胞因子失调。在这些脂肪因子中，瘦素通过多种途径发挥作用，包括参与细胞生长的 STAT3、MAPK 和 PI3K 途径。脂肪连接素对肿瘤生长的作用与瘦素相反，部分原因是增加了 p53 和 Bax 的凋亡反应。Visfatin 可通过 ERK1/2、PI3K/AKT 和 p38 增加癌细胞的增殖，而促炎细胞因子会刺激 ERK1/2、PI3K/AKT 和 p38。Omentin 通过 PI3K/Akt-Nos 途径参与癌症-肿瘤的发展。Apelin可能通过血管生成参与肿瘤进展。PAI-1 通过其对细胞粘附的抗纤维蛋白溶解活性和 uPA/uPAR 活性影响癌细胞的生长。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.