Cross-Talk between Adiponectin and IGF-IR in Breast Cancer

Mauro, Loredana; Naimo, Giuseppina Daniela; Ricchio, Emilia; Panno, Maria Luisa; Andò, Sebastiano

doi:10.3389/fonc.2015.00157

Cited by 50 publications

(63 citation statements)

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“…For the combined cases, the average beta was 0.25 (SD = 0.10, 95 % CI = 0.21–0.30) in low BMI cases and 0.35 (SD = 0.12, 95 % CI = 0.30–0.41) in high BMI cases and for the HGD/EAC cases, average beta was 0.20 (SD = 0.08, 95 % CI = 0.12–0.27) in low BMI cases and 0.38 (SD = 0.11, 95 % CI = 0.30–0.47) in high BMI cases. Of interest, adiponectin and leptin have also been implicated in obesity-associated cancer [34, 35]; however, we did not observe any differences in the DNA methylation status of genes involved in leptin or adiponectin pathways in any of the esophageal tissue sets in the high vs. low BMI subjects.…”

Section: Resultscontrasting

confidence: 80%

Global DNA methylation patterns in Barrett’s esophagus, dysplastic Barrett’s, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use

et al. 2016

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BackgroundThe risk of developing Barrett’s esophagus (BE) and/or esophageal adenocarcinoma (EAC) is associated with specific demographic and behavioral factors, including gender, obesity/elevated body mass index (BMI), and tobacco use. Alterations in DNA methylation, an epigenetic modification that can affect gene expression and that can be influenced by environmental factors, is frequently present in both BE and EAC and is believed to play a role in the formation of BE and its progression to EAC. It is currently unknown whether obesity or tobacco smoking influences the risk of developing BE/EAC via the induction of alterations in DNA methylation. To investigate this possibility, we assessed the genome-wide methylation status of 81 esophageal tissues, including BE, dysplastic BE, and EAC epithelia using HumanMethylation450 BeadChips (Illumina).ResultsWe found numerous differentially methylated loci in the esophagus tissues when comparing males to females, obese to lean individuals, and smokers to nonsmokers. Differences in DNA methylation between these groups were seen in a variety of functional genomic regions and both within and outside of CpG islands. Several cancer-related pathways were found to have differentially methylated genes between these comparison groups.ConclusionsOur findings suggest obesity and tobacco smoking may influence DNA methylation in the esophagus and raise the possibility that these risk factors affect the development of BE, dysplastic BE, and EAC through influencing the epigenetic status of specific loci that have a biologically plausible role in cancer formation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0273-7) contains supplementary material, which is available to authorized users.

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Section: Resultscontrasting

confidence: 80%

Global DNA methylation patterns in Barrett’s esophagus, dysplastic Barrett’s, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use

et al. 2016

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“…Recently, cross-talk between IGF-1 and adiponectin has been found to be associated with breast cancer 38. Mauro et al demonstrated that low levels of adiponectin induce cellular growth independently of IGF-1 in estrogen receptor alpha-positive breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of reduced dietary fat on estradiol, adiponectin, and IGF-1 levels in postmenopausal women with breast cancer

Murillo-Ortíz

Martı́nez-Garza

Landeros

et al. 2017

BCTT

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IntroductionIn recent years, epidemiological studies have strongly related obesity with an increased risk of developing postmenopausal breast cancer. The aromatization of fatty tissue increases the levels of estradiol and adiponectin, which is correlated with the body mass index (BMI). It is of interest to investigate the effect of reducing BMI on estradiol, adiponectin, and IGF-1, as reducing BMI could be a new strategy to limit the risk of recurrence during the adjuvant treatment of breast cancer.ObjectiveThe aim of this study is to investigate the effect of reduced dietary fat on the levels of serum estradiol, adiponectin, and IGF-1 among postmenopausal Mexican women with breast cancer.MethodsIn this controlled clinical trial, 100 female patients were randomly divided into two groups and followed for six months. Group 1 (n = 50) was subjected to reduced dietary fat, whereas Group 2 (n = 50) was subjected to a control diet. The levels of serum estradiol and testosterone were determined using an enzyme-linked immunosorbent assay, whereas the concentrations of adiponectin and IGF-1 were determined using a radioimmunoassay.ResultsThe patients subjected to reduced dietary fat showed a significant difference in BMI (27.93 ± 4.45 vs 26.05 ± 2.65; p = 0.01) and waist circumference (99.92 vs 91.59 cm; p = 0.0001) after the treatment. Moreover, a significant decrease in serum estradiol was observed (21.23 ± 14.32 vs 16.05 ± 10.25 ng/mL; p < 0.001). The adiponectin concentration also decreased significantly (47.53 ± 12.19 vs 42.52 ± 12.34 µg/mL; p = 0.004), while IGF-1 and testosterone did not show significant changes (p > 0.05). In addition, BMI had a relationship with serum adiponectin (r = −0.27; p = 0.02) and estradiol (r = 0.37; p = 0.001).ConclusionThe current study shows that reducing BMI decreases serum estradiol and adiponectin. Large clinical trials are needed to investigate the role of adiponectin in breast cancer development in obese women.

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“…Plasma levels of adiponectin are reduced in obesity in the abdomen, in the male, in postmenopausal women, in high blood pressure, hypertriglyceridemia in type 2 diabetes mellitus and coronary artery disease 71-77. Adiponectin expression is decreased by TNF-a and IL-6, increased by PPARy agonists 78 (Figure 6). Adiponectin exerts a reduction in the proliferation of adipocyte cells, endothelial cells and tumor cells 79,80.…”

Section: Introductionmentioning

confidence: 98%

Obesity and cancer: the role of adipose tissue and adipo-cytokines-induced chronic inflammation

et al. 2016

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Adipose tissue in addition to its ability to keep lipids is now recognized as a real organ with both metabolic and endocrine functions. Recent studies demonstrated that in obese animals is established a status of adipocyte hypoxia and in this hypoxic state interaction between adipocytes and stromal vascular cells contribute to tumor development and progression. In several tumors such as breast, colon, liver and prostate, obesity represents a poor predictor of clinical outcomes. Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro-inflammatory factors and a consequent alteration of key signaling mediators which may be an active local player in establishing the peritumoral environment promoting tumor growth and progression. Therefore, adipose tissue hypoxia might contribute to cancer risk in the obese population. To date the precise mechanisms behind this obesity-cancer link is not yet fully understood. In the light of information provided in this review that aims to identify the key mechanisms underlying the link between obesity and cancer we support that inflammatory state specific of obesity may be important in obesity-cancer link.

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Cross-Talk between Adiponectin and IGF-IR in Breast Cancer

Cited by 50 publications

References 100 publications

Global DNA methylation patterns in Barrett’s esophagus, dysplastic Barrett’s, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use

Global DNA methylation patterns in Barrett’s esophagus, dysplastic Barrett’s, and esophageal adenocarcinoma are associated with BMI, gender, and tobacco use

Effect of reduced dietary fat on estradiol, adiponectin, and IGF-1 levels in postmenopausal women with breast cancer

Obesity and cancer: the role of adipose tissue and adipo-cytokines-induced chronic inflammation

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