Human Adipose Tissue Macrophages Display Activation of Cancer-related Pathways

Mayi, Thérèse Hervèe; Daoudi, Mehdi; Derudas, Bruno; Gross, Barbara; Bories, Gaël; Wouters, Kristiaan; Brozek, John; Caïazzo, Robert; Raverdi, Violeta; Pigeyre, Marie; Allavena, Paola; Mantovani, Alberto; Pattou, François; Staels, Bart; Chinetti-Gbaguidi, Giulia

doi:10.1074/jbc.m111.315200

Cited by 61 publications

(27 citation statements)

References 41 publications

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“…that infiltrate adipose tissues in obese patients [69]. Interestingly, human adipose tissue macrophages resemble human tumor-associated macrophages and increase the expression of FAS in cancer cells, thus playing a critical role in cancer cell survival [70]. …”

Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

“…Biological mechanisms:hyperinsulinemia and insulin resistance [35, 41–45, 51, 52],IGF-I, IGF-II, and IGF binding proteins [35],sex hormones and sex hormone binding globulin [60–67],chronic whole body low-grade inflammation [96–100],adipose tissue inflammation [70],adipose tissue adipokine production (leptin, adiponectin, resistin, PAI-1, growth-related oncogenes, etc.) [71–78, 80–91, 94, 95],…”

Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

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Obesity as a Major Risk Factor for Cancer

2013

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The number of cancer cases caused by being obese is estimated to be 20% with the increased risk of malignancies being influenced by diet, weight change, and body fat distribution together with physical activity. Reports from the International Agency for Research into Cancer and the World Cancer Research Fund (WCRF) have shown that the strongest evidence exists for an association of obesity with the following cancer types: endometrial, esophageal adenocarcinoma, colorectal, postmenopausal breast, prostate, and renal, whereas the less common malignancies are leukemia, non-Hodgkin's lymphoma, multiple myeloma, malignant melanoma, and thyroid tumours. To be able to develop novel methods in prevention and treatment, we first must understand the underlying processes which link cancer to obesity. Four main systems have been identified as potential producers of cancer in obesity: insulin, insulin-like growth factor-I, sex steroids, and adipokines. Various novel candidate mechanisms have been proposed: chronic inflammation, oxidative stress, crosstalk between tumour cells and surrounding adipocytes, migrating adipose stromal cells, obesity-induced hypoxia, shared genetic susceptibility, and the functional defeat of immune function. Herein, we review the major pathogenic links between obesity and susceptibility to cancer.

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Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

Obesity as a Major Risk Factor for Cancer

2013

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“…This suggests that individual ATMs can bear both M1 and M2 characteristics simultaneously. Furthermore, M2 phenotypes, not M1 phenotypes, correlate with BMI in humans [58], and ATMs from obese human express the genetic signature of TAMs [59]. This suggests that obesity may induce the polarization of M2 macrophages, not M1 macrophages.…”

Section: Cellular Players In Obesity-induced At Inflammationmentioning

confidence: 99%

Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance

Lee

2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

594

496

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There is increasing evidence showing that inflammation is an important pathogenic mediator of the development of obesity-induced insulin resistance. It is now generally accepted that tissue-resident immune cells play a major role in the regulation of this obesity-induced inflammation. The roles that adipose tissue (AT)-resident immune cells play have been particularly extensively studied. AT contains most types of immune cells and obesity increases their numbers and activation levels, particularly in AT macrophages (ATMs). Other pro-inflammatory cells found in AT include neutrophils, Th1 CD4 T cells, CD8 T cells, B cells, DCs, and mast cells. However, AT also contains anti-inflammatory cells that counter the pro-inflammatory immune cells that are responsible for the obesity-induced inflammation in this tissue. These anti-inflammatory cells include regulatory CD4 T cells (Tregs), Th2 CD4 T cells, and eosinophils. Hence, AT inflammation is shaped by the regulation of pro- and anti-inflammatory immune cell homeostasis, and obesity skews this balance towards a more pro-inflammatory status. Recent genetic studies revealed several molecules that participate in the development of obesity-induced inflammation and insulin resistance. In this review, the cellular and molecular players that participate in the regulation of obesity-induced inflammation and insulin resistance are discussed, with particular attention being placed on the roles of the cellular players in these pathogeneses.

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“…Adipose tissue macrophages (ATM) enhance the levels of inflammatory markers dysregulated in cancer, suggesting that macrophages from peritumoral adipose tissue are locally involved in promoting carcinogenesis (129–131). The presence of tumor-associated macrophages (TAM) also contributes to the pro-inflammatory tumor environment.…”

Section: Pathophysiological Mechanisms Relating Visceral Adipose Tissmentioning

confidence: 99%

Mechanisms Linking Excess Adiposity and Carcinogenesis Promotion

et al. 2014

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Obesity constitutes one of the most important metabolic diseases being associated to insulin resistance development and increased cardiovascular risk. Association between obesity and cancer has also been well established for several tumor types, such as breast cancer in post-menopausal women, colorectal, and prostate cancer. Cancer is the first death cause in developed countries and the second one in developing countries, with high incidence rates around the world. Furthermore, it has been estimated that 15–20% of all cancer deaths may be attributable to obesity. Tumor growth is regulated by interactions between tumor cells and their tissue microenvironment. In this sense, obesity may lead to cancer development through dysfunctional adipose tissue and altered signaling pathways. In this review, three main pathways relating obesity and cancer development are examined: (i) inflammatory changes leading to macrophage polarization and altered adipokine profile; (ii) insulin resistance development; and (iii) adipose tissue hypoxia. Since obesity and cancer present a high prevalence, the association between these conditions is of great public health significance and studies showing mechanisms by which obesity lead to cancer development and progression are needed to improve prevention and management of these diseases.

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Human Adipose Tissue Macrophages Display Activation of Cancer-related Pathways

Cited by 61 publications

References 41 publications

Obesity as a Major Risk Factor for Cancer

Obesity as a Major Risk Factor for Cancer

Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance

Mechanisms Linking Excess Adiposity and Carcinogenesis Promotion

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