IL‐10 suppresses TNF‐α‐induced expression of human aromatase gene in mammary adipose tissue

Martínez‐Chacón, Gabriela; Brown, Kristy A.; Docanto, Maria; Kumar, Himanshu; Salminen, Seppo; Saarinen, Niina M.; Mäkelä, Sari

doi:10.1096/fj.201700938rrr

Cited by 24 publications

(29 citation statements)

References 58 publications

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“…Higher aromatase levels were detected in breast tissue with inflammation in postmenopausal women, independently of BMI (17). Interleukin 10, an antiinflammatory cytokine, reportedly suppressed aromatase levels in human adipose tissue (19). Moreover, blocking inflammation in adipose tissue suppresses breast cancer progression (20).…”

Section: Discussionmentioning

confidence: 98%

Breast Cancer in Lean Postmenopausal Women Might Have Specific Pathological Features

Uomori¹,

Horimoto²,

Arakawa³

et al. 2019

In Vivo

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Background/Aim: The rate of obesity, an independent risk factor for breast cancer in post-menopausal women, is quite low in Japan, indicating breast cancer in lean women to be more common in the Japanese than in Westerners. However, biological characteristics of such breast cancers have not been adequately investigated. Patients and Methods: We retrospectively investigated clinicopathological breast cancer features of 566 postmenopausal Japanese women, who underwent curative surgery, in relation to patient physique based on the body mass index. Results: There were no differences in several factors examined such as tumour size according to patient physique. On the other hand, mean values of the Ki67 labelling index were significantly higher in lean compared to obese patients (p=0.027). Likewise, HER2-positive tumours were more often observed in lean patients (p=0.051). Conclusion: Lean postmenopausal women had more aggressive tumours, apparently contradicting the widely held view for breast cancer in obese women.

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Section: Discussionmentioning

confidence: 98%

Breast Cancer in Lean Postmenopausal Women Might Have Specific Pathological Features

Uomori¹,

Horimoto²,

Arakawa³

et al. 2019

In Vivo

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“…Promoter I.4specific transcripts, present in adipose tissue, can be stimulated by inflammatory mediators, including IL-6, IL-11, leukemia inhibitory factor, oncostatin M, as well as TNFα [51,52]. Using preclinical models and human breast tissue, the TNFα-mediated induction of aromatase was shown to require ERK1/2 activation, an effect that was blocked by the antiinflammatory cytokine IL-10 [53]. Taken together, these studies propose new mechanisms that explain the elevation in estrogen produced by breast adipose tissue in obese postmenopausal women.…”

Section: Aromatase Regulation In Obesitymentioning

confidence: 99%

Estrogens and breast cancer: Mechanisms involved in obesity-related development, growth and progression

Bhardwaj

Benito-Martín

et al. 2019

The Journal of Steroid Biochemistry and Molecular Biology

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138

104

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Obesity is a risk factor for estrogen receptor-positive (ER+) breast cancer after menopause. The pro-proliferative effects of estrogens are well characterized and there is a growing body of evidence to also suggest an important role in tumorigenesis. Importantly, obesity not only increases the risk of breast cancer, but it also increases the risk of recurrence and cancer-associated death. Aromatase is the rate-limiting enzyme in estrogen biosynthesis and its expression in breast adipose stromal cells is hypothesized to drive the growth of breast tumors and confer resistance to endocrine therapy in obese postmenopausal women. The molecular regulation of aromatase has been characterized in response to many obesity-related molecules, including inflammatory mediators and adipokines. This review is aimed at providing an overview of our current knowledge in relation to the regulation of estrogens in adipose tissue and their role in driving breast tumor development, growth and progression.

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“…TNF-α released by M1 macrophages can promote metastasis and inhibit apoptosis of ovarian cancer cells by activating the signaling pathway of NF-κB (80). TNF-α is also a key factor driving the expression of the aromatase gene, and IL-10 can regulate the expression of aromatase in adipose tissue by inhibiting the TNF-α signaling pathway (81). Moreover, TNF-α could induce serine phosphorylation of IRS-1 and inhibit its triggering of downstream signals, leading to insulin resistance.…”

Section: Molecular and Metabolic Mechanisms Underlying The Obesity-enmentioning

confidence: 99%

The Role of Metabolic Syndrome in Endometrial Cancer: A Review

Yang

Wang

2019

Front. Oncol.

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Endometrial cancer is one of the most common cancers of the female reproductive system. Although surgery, radiotherapy, chemotherapy, and hormone therapy can significantly improve the survival of patients, the treatment of patients with very early lesions and a strong desire to retain reproductive function or late recurrence is still in the early stages. Metabolic syndrome (MS) is a clustering of at least three of the five following medical conditions: central obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL). Obesity, diabetes and hypertension often coexist in patients with endometrial cancer, which increases the risk of endometrial cancer, also known as the “triple syndrome of endometrial cancer.” In recent years, epidemiological and clinical studies have found that MS associated with metabolic diseases is closely related to the incidence of endometrial cancer. However, the key molecular mechanisms underlying the induction of endometrial cancer by MS have not been elucidated to date. Characterizing the tumor metabolism microenvironment will be advantageous for achieving a comprehensive view of the molecular mechanism of metabolic syndrome associated with endometrial cancer and for providing a new target for the treatment of endometrial cancer. This review focuses on recent advances in determining the role of metabolic syndrome-related factors and mechanisms in the pathogenesis of endometrial cancer. We suggest that interfering with the tumor metabolic microenvironment-related molecular signals may inhibit the occurrence of endometrial cancer.

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IL‐10 suppresses TNF‐α‐induced expression of human aromatase gene in mammary adipose tissue

Cited by 24 publications

References 58 publications

Breast Cancer in Lean Postmenopausal Women Might Have Specific Pathological Features

Breast Cancer in Lean Postmenopausal Women Might Have Specific Pathological Features

Estrogens and breast cancer: Mechanisms involved in obesity-related development, growth and progression

The Role of Metabolic Syndrome in Endometrial Cancer: A Review

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