Effects of estrogen on breast cancer development: Role of estrogen receptor independent mechanisms

Yue, Wei; Wang, Ji Ping; Li, Yuebai; Fan, Ping; Liu, Guijian; Zhang, Nan; Conaway, Mark R.; Wang, Hongkun; Korach, Kenneth S.; Bocchinfuso, Wayne P.; Santen, Richard J.

doi:10.1002/ijc.25207

Cited by 144 publications

(101 citation statements)

References 67 publications

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“…Epidemiological and clinical data show that the ER plays an important role in breast cancer development 125, 126, 127. More than 65% of all breast cancers are ER‐positive 128.…”

Section: Mechanisms Underlying Bpa‐stimulated Carcinogenic Effectsmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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Breast cancer is the fifth most common cause of cancer death in the world and the second most common fatal cancer in women. Epidemiological studies and clinical data have indicated that hormones, including estrogen, progesterone, and prolactin, play important roles in the initiation and progression of breast cancer. Bisphenol A (BPA) is one of the most commonly used and thoroughly studied endocrine disruptors. It can be released from consumer products and deposited in the environment, thus creating potential for human exposure through oral, inhaled, and dermal routes. Some recent reviews have summarized the known mechanisms of endocrine disruptions by BPA in human diseases, including obesity, reproductive disorders, and birth defects. However, large knowledge gaps still exist on the roles BPA may play in cancer initiation and development. Evidence from animal and in vitro studies has suggested an association between increased incidence of breast cancer and BPA exposure at doses below the safe reference doses that are the most environmentally relevant. Most current studies have paid little attention to the cancer‐promoting properties of BPA at low doses. In this review, recent findings on the carcinogenic effects of low‐dose BPA on breast cancer and discussed possible biologic mechanisms are summarized.

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“…Epidemiological and clinical data show that the ER plays an important role in breast cancer development 125, 126, 127. More than 65% of all breast cancers are ER‐positive 128.…”

Section: Mechanisms Underlying Bpa‐stimulated Carcinogenic Effectsmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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“…Additionally, ERa directly binds to Gai and Gbg (Kumar et al 2007). However, some rapid effects of estrogens are transduced by ER-independent pathways (Santen et al 2009, Yue et al 2010, Haas et al 2012, Richardson et al 2012. Another cell-surface receptor for estrogen has been identified as the orphan G protein-coupled receptor GPR30.…”

Section: Estrogen Receptors In the Thyroid Glandmentioning

confidence: 99%

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fortunato¹,

Ferreira²,

Hecht³

et al. 2014

Journal of Endocrinology

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Thyroid diseases, such as autoimmune disease and benign and malignant nodules, are more prevalent in women than in men, but the mechanisms involved in this sex difference is still poorly defined. H 2 O 2 is produced at high levels in the thyroid gland and regulates parameters such as cell proliferation, migration, survival, and death; an imbalance in the cellular oxidant-antioxidant system in the thyroid may contribute to the greater incidence of thyroid disease among women. Recently, we demonstrated the existence of a sexual dimorphism in the thyrocyte redox balance, characterized by higher H 2 O 2 production, due to higher NOX4 and Poldip2 expression, and weakened enzymatic antioxidant defense in the thyroid of adult female rats compared with male rats. In addition, 17b-estradiol administration increased NOX4 mRNA expression and H 2 O 2 production in thyroid PCCL3 cells. In this review, we discuss the possible involvement of oxidative stress in estrogenrelated thyroid pathophysiology. Our current hypothesis suggests that a redox imbalance elicited by estrogen could be involved in the sex differences found in the prevalence of thyroid dysfunctions.

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“…The ERKO/Wnt-1 transgenic mouse demonstrates the importance of these metabolites in tumor initiation. In this study treating ERKO/Wnt-1 transgenic mice with E2 increased mammary carcinogenesis in the absence of ER-α, thus implicating the metabolites as the culprits [ 56 ].…”

Section: Role Of Estrogen In Mammary Gland Development and Breast Cancermentioning

confidence: 96%

Fetal Alcohol Exposure and Mammary Tumorigenesis in Offspring: Role of the Estrogen and Insulin-Like Growth Factor Systems

Cohick

Crismale-Gann

Stires

et al. 2014

Biological Basis of Alcohol-Induced Cancer

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Fetal alcohol spectrum disorders affect a significant number of live births each year, indicating that alcohol consumption during pregnancy is an important public health issue. Environmental exposures and lifestyle choices during pregnancy may affect the offspring's risk of disease in adulthood, leading to the idea that a woman's risk of breast cancer may be pre-programmed prior to birth. Exposure of pregnant rats to alcohol increases tumorigenesis in the adult offspring in response to mammary carcinogens. The estrogen and insulin-like growth factor (IGF-I) axes occupy central roles in normal mammary gland development and breast cancer. 17-β estradiol (E2) and IGF-I synergize to regulate formation of terminal end buds and ductal elongation during pubertal development. The intracellular signaling pathways mediated by the estrogen and IGF-I receptors cross-talk at multiple levels through both genomic and non-genomic mechanisms. Several components of the E2 and IGF-I systems are altered in early development in rat offspring exposed to alcohol in utero, therefore, these changes may play a role in the enhanced susceptibility to mammary carcinogens observed in adulthood. Alcohol exposure in utero induces a number of epigenetic alterations in non-mammary tissues in the offspring and other adverse in utero exposures induce epigenetic modifications in the mammary gland. Future studies will determine if fetal alcohol exposure can induce epigenetic modifications in genes that regulate E2/IGF action at key phases of mammary development, ultimately leading to changes in susceptibility to carcinogens.

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Effects of estrogen on breast cancer development: Role of estrogen receptor independent mechanisms

Cited by 144 publications

References 67 publications

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fetal Alcohol Exposure and Mammary Tumorigenesis in Offspring: Role of the Estrogen and Insulin-Like Growth Factor Systems

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