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      Expression of AdipoR1 and AdipoR2 Receptors as Leptin-Breast Cancer Regulation Mechanisms

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          Abstract

          The development of breast cancer is influenced by the adipose tissue through the proteins leptin and adiponectin. However, there is little research concerning AdipoR1 and AdipoR2 receptors and the influence of leptin over them. The objective of this work was to analyze the expression of AdipoR1 and AdipoR2, modulated by differential concentrations of leptin in an obesity model (10 ng/mL, 100 ng/mL, and 1000 ng/mL) associated with breast cancer in MCF-7 and HCC1937 cell lines. Each cell line was characterized through immunohistochemistry, and the expression of AdipoR1 and AdipoR2 was analyzed by PCR in real time using TaqMan® probes. Leptin induced an increase in cell population of MCF-7 (23.8%, 10 ng/mL, 48 h) and HCC1937 (17.24%, 1000 ng/mL, 72 h). In MCF-7, the expression of AdipoR1 decreased (3.81%, 1000 ng/mL) and the expression of AdipoR2 increased by 13.74 times (10 ng/mL) with regard to the control. In HCC1937, the expression of AdipoR1 decreased by 86.28% (10 ng/mL), as well as the expression of AdipoR2 (50.3%, 100 ng/mL). In regard to the results obtained, it could be concluded that leptin has an effect over the expression of AdipoR1 and AdipoR2 mRNA.

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          Molecular links between obesity and breast cancer.

          S Sukumar, A Lorincz (2006)
          Breast cancer continues to be a major health problem for women in the USA and worldwide. There is a need to identify and take steps to alter modifiable breast cancer risks. Conditions of obesity and overweight are risk factors that have reached epidemic proportions. This article reviews the evidence in the literature that test mechanism-based hypotheses which attempt to provide a molecular basis for a causal link between obesity and breast cancer risk, particularly the effects of metabolic syndrome and insulin resistance, peripheral estrogen aromatization in adipose tissue, and direct effect of adipokines. Future areas for study and implications for therapy are discussed.
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            Adiponectin receptor signalling in the brain.

            Thiruma V. Arumugam, Christopher Sobey, John Thundyil … (2011)
            Adiponectin is an important adipocyte-derived hormone that regulates metabolism of lipids and glucose, and its receptors (AdipoR1, AdipoR2, T-cadherin) appear to exert actions in peripheral tissues by activating the AMP-activated protein kinase, p38-MAPK, PPARα and NF-kappa B. Adiponectin has been shown to exert a wide range of biological functions that could elicit different effects, depending on the target organ and the biological milieu. There is substantial evidence to suggest that adiponectin receptors are expressed widely in the brain. Their expression has been detected in regions of the mouse hypothalamus, brainstem, cortical neurons and endothelial cells, as well as in whole brain and pituitary extracts. While there is now considerable evidence for the presence of adiponectin and its receptors in the brain, their precise roles in brain diseases still remain unclear. Only a few research studies have looked at this facet of adiponectins in brain disorders. This brief review will describe the evidence for important functions by adiponectin, its structure and known actions, evidence for expression of AdipoRs in the brain, their involvement in brain disorders and the therapeutic potential of agents that could modify AdipoR signalling. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
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              Obesity, body size, and risk of postmenopausal breast cancer: the Women's Health Initiative (United States).

              Libby Morimoto, Emily White, Z. Chen … (2002)
              Body size is an important modifiable risk factor for breast cancer. Although obesity has generally been found to be associated with increased risk for postmenopausal breast cancer, there remain questions concerning the role of body fat distribution, lifetime weight history, and effects within specific subgroups of women. We assessed the relationship of several anthropometric measures and risk of postmenopausal breast cancer in 85,917 women aged 50-79 at entry in the Women's Health Initiative Observational Study. Women were enrolled during 1993-1998 at 40 clinics in the US and 1030 developed invasive breast cancer by April 2000. Upon entry, trained clinical center staff measured each woman's height, weight, and waist and hip circumference. Anthropometric factors were not associated with breast cancer among women who had ever used hormone replacement therapy (HRT). Among HRT non-users, heavier women (baseline body mass index (BMI) >31.1) had an elevated risk of postmenopausal breast cancer (relative risk (RR) = 2.52; 95% confidence interval (CI) = 1.62-3.93), compared to slimmer women (baseline BMI < 22.6). The elevation in risk associated with increasing BMI appeared to be most pronounced among younger postmenopausal women. Change in BMI since age 18, maximum BMI, and weight were also associated with breast cancer in HRT non-users. While both waist and hip circumference were associated with breast cancer risk, their ratio, a measure of fat distribution, was not (RR = 1.33; 95% CI = 0.88-2.01). Our study confirms previously reported findings that generalized obesity is an important risk factor for postmenopausal breast cancer, but only among women who have never taken HRT. Lifetime weight gain is also a strong predictor of breast cancer. Waist to hip ratio, a measure of weight distribution, does not appear to be related to postmenopausal breast cancer risk.
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                Author and article information

                Contributors
                Jonnathan Guadalupe Santillán-Benítez:
                ORCID: http://orcid.org/0000-0003-3574-1231
                Journal
                Journal ID (nlm-ta): Dis Markers
                Journal ID (iso-abbrev): Dis. Markers
                Journal ID (publisher-id): DM
                Title: Disease Markers
                Publisher: Hindawi
                ISSN (Print): 0278-0240
                ISSN (Electronic): 1875-8630
                Publication date (Print): 2017
                Publication date (Electronic): 5 September 2017
                Volume: 2017
                Electronic Location Identifier: 4862016
                Affiliations
                1Faculty of Chemistry, Autonomous University of the State of Mexico (UAEMex), Toluca, MEX, Mexico
                2Specialized Hemato-Oncological Laboratory of the Children's Hospital, IMIEM, Toluca, MEX, Mexico
                3Molecular Biology Laboratory, Medical Research Center (CICMED), Toluca, MEX, Mexico
                4Laboratory of Immunohistochemistry, National Pediatrics Institute, Coyoacán, MEX, Mexico
                Author notes

                Academic Editor: Stefano M. M. Basso

                Author information
                http://orcid.org/0000-0003-3574-1231
                http://orcid.org/0000-0003-0793-0940
                http://orcid.org/0000-0001-6431-8497
                Article
                DOI: 10.1155/2017/4862016
                PMC ID: 5605926
                SO-VID: 694efe51-52a7-4cde-b0af-1d9c3db10279
                Copyright © Copyright © 2017 Martha Daniela Mociño-Rodríguez et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 May 2017
                Date accepted : 20 July 2017
                Funding
                Funded by: IMIEM Specialized Hemato-Oncological Laboratory
                Funded by: Universidad Autónoma del Estado de México
                Categories
                Subject: Research Article

                Data availability:

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