Leptin, adipocytes and breast cancer: Focus on inflammation and anti-tumor immunity

Delort, Laëtitia; Rossary, Adrien; Farges, Marie‐Chantal; Vasson, Marie‐Paule; Caldefie-Chézet, Florence

doi:10.1016/j.lfs.2015.04.012

Cited by 75 publications

(59 citation statements)

References 129 publications

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“…Higher aromatase activity and higher degrees of obesity may abate the efficacy of aromatase inhibitors 204. Leptin, an adipocyte-derived cytokine, would arouse proliferation in some cell types, such as mammary epithelium, which has an effect on the neoplasm cell proliferation, apoptosis, and cell cycle 205-207. Data has shown that high glucose levels can induce leptin signaling directly 208.…”

Section: Adipose Cellsmentioning

confidence: 99%

Role of tumor microenvironment in tumorigenesis

et al. 2017

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Tumorigenesis is a complex and dynamic process, consisting of three stages: initiation, progression, and metastasis. Tumors are encircled by extracellular matrix (ECM) and stromal cells, and the physiological state of the tumor microenvironment (TME) is closely connected to every step of tumorigenesis. Evidence suggests that the vital components of the TME are fibroblasts and myofibroblasts, neuroendocrine cells, adipose cells, immune and inflammatory cells, the blood and lymphatic vascular networks, and ECM. This manuscript, based on the current studies of the TME, offers a more comprehensive overview of the primary functions of each component of the TME in cancer initiation, progression, and invasion. The manuscript also includes primary therapeutic targeting markers for each player, which may be helpful in treating tumors.

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Section: Adipose Cellsmentioning

confidence: 99%

Role of tumor microenvironment in tumorigenesis

et al. 2017

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“…Leptin is known to be pro-tumorigenic and to act directly on breast epithelial cells to promote proliferation, by promoting estrogen signaling, activation of MAPKs and STAT3 signaling, and inhibition of apoptosis by activation of AKT signaling [46]. Leptin is also pro-angiogenic and has been shown to promote epithelial-mesenchymal transition (EMT) in breast cancer and to promote the self-renewal of mammary stem cells and breast cancer stem cells [47–49].…”

Section: Obesity and Cancermentioning

confidence: 99%

Obesity and cancer: inflammation bridges the two

Kolb

Sutterwala

Zhang

2016

Current Opinion in Pharmacology

321

228

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Obesity is a growing public health problem and affects 35% US adults. Obesity increases the risk of many cancer types and is associated with poor outcomes. Clinical management of cancer patients has been essentially the same between normal weight and obese individuals. Understanding causal mechanisms by which obesity drives cancer initiation and progression is essential for the development of novel precision therapy for obese cancer patients. One caveat is that various mechanisms have been proposed for different cancer types for their progression under obesity. Since obesity is known to have global impact on inflammation, here we will summarize recent literature and discuss the potential of inflammation being the common causal mechanism to promote cancer promotion across cancer types.

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“…Adipocytes alter breast cancer cell growth, migration, and invasion in vitro [9, 12, 13]. However, most attention to date has focused on the production of hormones, growth factors, and cytokines by adipose tissue in tumor progression (see review [14]). Relatively, little attention has been paid to the significant potential for stromal adipocytes to provide metabolic substrates, thereby supporting breast cancer progression.…”

Section: Introductionmentioning

confidence: 99%

Adipocyte lipolysis links obesity to breast cancer growth: adipocyte-derived fatty acids drive breast cancer cell proliferation and migration

et al. 2017

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BackgroundObesity is associated with increased recurrence and reduced survival of breast cancer. Adipocytes constitute a significant component of breast tissue, yet their role in provisioning metabolic substrates to support breast cancer progression is poorly understood.ResultsHere, we show that co-culture of breast cancer cells with adipocytes revealed cancer cell-stimulated depletion of adipocyte triacylglycerol. Adipocyte-derived free fatty acids were transferred to breast cancer cells, driving fatty acid metabolism via increased CPT1A and electron transport chain complex protein levels, resulting in increased proliferation and migration. Notably, fatty acid transfer to breast cancer cells was enhanced from “obese” adipocytes, concomitant with increased stimulation of cancer cell proliferation and migration. This adipocyte-stimulated breast cancer cell proliferation was dependent on lipolytic processes since HSL/ATGL knockdown attenuated cancer cell responses.ConclusionsThese findings highlight a novel and potentially important role for adipocyte lipolysis in the provision of metabolic substrates to breast cancer cells, thereby supporting cancer progression.Electronic supplementary materialThe online version of this article (doi:10.1186/s40170-016-0163-7) contains supplementary material, which is available to authorized users.

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Leptin, adipocytes and breast cancer: Focus on inflammation and anti-tumor immunity

Cited by 75 publications

References 129 publications

Role of tumor microenvironment in tumorigenesis

Role of tumor microenvironment in tumorigenesis

Obesity and cancer: inflammation bridges the two

Adipocyte lipolysis links obesity to breast cancer growth: adipocyte-derived fatty acids drive breast cancer cell proliferation and migration

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