Leptin and Adiponectin: Emerging Therapeutic Targets in Breast Cancer

Surmacz, Eva

doi:10.1007/s10911-013-9302-8

Cited by 73 publications

(54 citation statements)

References 148 publications

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“…ObR expression has been detected in human breast cancers, most notably in human breast cancer subtypes that carry a worse prognosis. High expression of ObR in breast tumors is associated with a poor prognosis particularly in patients with elevated circulating leptin levels (180). Its expression has also been found in gastrointestinal cancers, and in some tumors, it is associated with a worse prognosis.…”

Section: Adipokinesmentioning

confidence: 99%

Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality

Gallagher

2015

Physiological Reviews

624

434

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Obesity and type 2 diabetes are becoming increasingly prevalent worldwide, and both are associated with an increased incidence and mortality from many cancers. The metabolic abnormalities associated with type 2 diabetes develop many years before the onset of diabetes and, therefore, may be contributing to cancer risk before individuals are aware that they are at risk. Multiple factors potentially contribute to the progression of cancer in obesity and type 2 diabetes, including hyperinsulinemia and insulin-like growth factor I, hyperglycemia, dyslipidemia, adipokines and cytokines, and the gut microbiome. These metabolic changes may contribute directly or indirectly to cancer progression. Intentional weight loss may protect against cancer development, and therapies for diabetes may prove to be effective adjuvant agents in reducing cancer progression. In this review we discuss the current epidemiology, basic science, and clinical data that link obesity, diabetes, and cancer and how treating obesity and type 2 diabetes could also reduce cancer risk and improve outcomes.

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Section: Adipokinesmentioning

confidence: 99%

Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality

Gallagher

2015

Physiological Reviews

624

434

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“…Actions of adiponectin in breast cancer lines that express AdipoR1/R2 include reduce cancer invasion and migration to other cells [62]. Research demonstrates adiponectin is anti-carcinogenic in breast cancer cell lines, including MCF-7, MDA-MB-231 and T47D through its antiproliferative properties [63].…”

Section: Adiponectinmentioning

confidence: 99%

“…Adiponectin also reduces the bioavailability of certain growth factors, such as platelet-derived growth factor BB (PDGF-BB), basic fibroblast growth factor (FGF), and heparin-binding epidermal growth factor-like growth factor (HB EGF) [68]. Therapeutic targets of breast cancer include therapies that activate the signaling or mimic the actions of adiponectin such as Metformin, PPARγ agonists and activators of AMPK signaling pathway [62].…”

Section: Adiponectinmentioning

confidence: 99%

Adipose tissue, obesity and adipokines: role in cancer promotion

Booth

Magnuson

Fouts

et al. 2015

Hormone Molecular Biology and Clinical Investigation

239

235

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Adipose tissue is a complex organ with endocrine, metabolic and immune regulatory roles. Adipose depots have been characterized to release several adipocytokines that work locally in an autocrine and paracrine fashion or peripherally in an endocrine fashion. Adipocyte hypertrophy and excessive adipose tissue accumulation, as occurs during obesity, dysregulates the microenvironment within adipose depots and systemically alters peripheral tissue metabolism. The term "adiposopathy" is used to describe this promotion of pathogenic adipocytes and associated adipose -elated disorders. Numerous epidemiological studies confirm an association between obesity and various cancer forms. Proposed mechanisms that link obesity/adiposity to high cancer risk and mortality include, but are not limited to, obesity-related insulin resistance, hyperinsulinemia, sustained hyperglycemia, glucose intolerance, oxidative stress, inflammation and/or adipocktokine production. Several epidemiological studies have demonstrated a relationship between specific circulating adipocytokines and cancer risk. The aim of this review is to define the function, in normal weight and obesity states, of wellcharacterized and novel adipokines including leptin, adiponectin, apelin, visfatin, resistin, chemerin, omentin, nesfatin and vaspin and summarize the data that relates their dysfunction, whether associated or direct effects, to specific cancer outcomes. Overall research suggests most adipokines promote cancer cell progression via enhancement of cell proliferation and migration, inflammation and anti-apoptosis pathways, which subsequently can prompt cancer metastasis. Further research and longitudinal studies are needed to define the specific independent and additive roles of adipokines in cancer progression and reoccurrence.

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“…The induction of leptin responses and effects involves its binding to leptin receptor b (ObR), leading to the activation of intracellular signals through JAK2, STAT3, and AMPK (Kwon & Pessin 2013). These molecules will then regulate several pathways of pivotal importance to cancers, such as the AKT/mTOR/PI3K and ERK/MAPK pathways, involved in cell growth and survival; COX2, IL1, and NFkB, related to inflammation; and VEGFs, involved in angiogenesis (Surmacz 2013). Thus, leptin interacts with several factors that participate in diverse carcinogenic stages, and its relationship with breast, prostate, colorectal, hepatocellular, pancreatic, and lung cancers, as well as thyroid cancer, has consistently been demonstrated in the literature (Dutta et al 2012, Vansaun 2013.…”

Section: Inflammationmentioning

confidence: 99%

Obesity and thyroid cancer

Marcello,

Cunha,

Batista

et al. 2014

Endocrine Related Cancer

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Many studies have provided observational data on the association of obesity and thyroid cancers, but only few of them propose mechanisms that would permit a better understanding of the causal molecular mechanisms of this association. Considering that there is an increasing incidence of both obesity and thyroid cancers, we need to summarize and link recent studies in order to characterize and understand the contribution of obesity-related factors that might affect thyroid cancer development and progression. Adipose tissue is involved in many vital processes, including insulin sensitivity, angiogenesis, regulation of energy balance, activation of the complement system, and responses such as inflammation. Although these processes have their own molecular pathways, they involve the same molecules through which obesity and adipose tissue might exert their roles in carcinogenesis, not only affecting MAPK and PI3K or even insulin pathways, but also recruiting local inflammatory responses that could result in disease formation and progression. This review describes five important issues that might explain the link between excessive weight and thyroid cancer: thyroid hormones, insulin resistance, adipokines, inflammation, and sexual hormones.

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Leptin and Adiponectin: Emerging Therapeutic Targets in Breast Cancer

Cited by 73 publications

References 148 publications

Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality

Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality

Adipose tissue, obesity and adipokines: role in cancer promotion

Obesity and thyroid cancer

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