Research Resource: Estrogen-Driven Prolactin-Mediated Gene-Expression Networks in Hormone-Induced Prostatic Intraepithelial Neoplasia

Tam, Neville N.C.; Szeto, Carol Y.Y.; Freudenberg, Johannes; Fullenkamp, Amy N.; Medvedovic, Mario; Ho, Shuk‐Mei

doi:10.1210/jcem.95.10.9995

Cited by 2 publications

(2 citation statements)

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“…In vitro studies on rat prostate models have shown that estrogen could induce genotoxicity via single strand DNA breaks and lipid peroxidation . Another study demonstrated that chronic exposure to estrogen increased circulating prolactin levels in adult human whereas proliferative effects of prolactin has been well identified, and recent studies have supported the role of prolactin in breast and prostate cancers development . On the other hand, estrogen functions are mediated by the estrogen specific receptors (ER), and multiple ERs are localized in prostate tissues that their activation has been associated with in vitro and in vivo phenotypic changes.…”

Section: Mechanisms Of Obesity‐related Cancermentioning

confidence: 99%

From obesity to cancer: a review on proposed mechanisms

Tahergorabi

Khazaei

Moodi

et al. 2016

Cell Biochemistry & Function

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Nowadays, obesity is considered as a serious and growing global health problem. It is documented that the overweight and obesity are major risk factors for a series of noncommunicable diseases, and in recent years, the obesity-cancer link has received much attention. Numerous epidemiological studies have shown that obesity is associated with increased risk of several cancer types, including colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, gallbladder, and leukemia, and can also lead to poorer treatment. We review here the epidemiological and experimental evidences for the association between obesity and cancer. Specifically, we discuss potential mechanisms focusing how dysfunctional angiogenesis, chronic inflammation, interaction of proinflammatory cytokines, endocrine hormones, and adipokines including leptin, adiponectin insulin, growth factors, estrogen, and progesterone and strikingly, cell metabolism alteration in obesity participate in tumor development and progression, resistance to chemotherapy, and targeted therapies such as antiangiogenic and immune therapies.

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Section: Mechanisms Of Obesity‐related Cancermentioning

confidence: 99%

From obesity to cancer: a review on proposed mechanisms

Tahergorabi

Khazaei

Moodi

et al. 2016

Cell Biochemistry & Function

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“…Prolactin is an E2‐inducible gene and an important downstream effector in many cell types. Prolactin has been reported to be involved in E2‐induced apoptosis in regressing postpartum rat corpora lutea (Goyeneche and Telleria ) and in E2‐induced prostate cancer (Tam et al ). To elucidate whether this hormone could contribute to some extent to E2‐driven sGCα1 up‐regulation, we studied the effect of 2 prolactin concentrations in the range of those observed in pregnancy or hyperprolactinemia (Majumdar and Mangal ).…”

Section: Discussionmentioning

confidence: 99%

Soluble Guanylyl Cyclase Alpha1 Subunit: A New Marker for Estrogenicity of Endocrine Disruptor Compounds

Pino

Ronchetti

Cordeiro

et al. 2019

Enviro Toxic and Chemistry

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Endocrine‐disrupting chemicals (EDCs) include widespread naturally occurring and synthetic substances in the environment that adversely affect humans and wildlife. Because of the increasing numbers of EDCs, screening methods and ideal biomarkers to determine EDC potencies at relevant environmental concentrations need to be drastically improved. Soluble guanylyl cyclase α1 subunit (sGCα1) is an abundant cytosolic protein ubiquitously expressed in most tissues. We previously showed that sGCα1 is specifically and highly up‐regulated by estrogen (E2) in vivo and in vitro, even though it lacks estrogen‐responsive elements. The aim of the present study was to evaluate sGCα1 protein expression as a potential marker for xenoestrogenic EDC exposure in the E2‐responsive lactosomatotroph‐derived pituitary cell line GH3. Cells were incubated with a wide variety of EDCs such as heavy metals and a metalloid, synthetic E2 derivatives, plastic byproducts, and pesticides at a range of doses including those with proven xenoestrogenic activity. We demonstrated that E2 increased sGCα1 expression in GH3 cells as well as in other E2‐responsive tumor cell lines. Moreover, this effect was fully dependent on estrogen receptor (ER) activation. Importantly, sGCα1 protein levels were strongly up‐regulated by all the EDCs tested, even by those exhibiting low or null ER binding capacity. We provide evidence that the in vitro sGCα1 protein assay may be a very sensitive and powerful tool to identify compounds with estrogenic activity, which could improve current mammalian‐based screening methods. Environ Toxicol Chem 2019;38:2719–2728. © 2019 SETAC

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Research Resource: Estrogen-Driven Prolactin-Mediated Gene-Expression Networks in Hormone-Induced Prostatic Intraepithelial Neoplasia

Cited by 2 publications

References 0 publications

From obesity to cancer: a review on proposed mechanisms

From obesity to cancer: a review on proposed mechanisms

Soluble Guanylyl Cyclase Alpha1 Subunit: A New Marker for Estrogenicity of Endocrine Disruptor Compounds

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