Stimulation of ovarian cell proliferation by tetrabromobisphenol A but not tetrachlorobisphenol A through G protein-coupled receptor 30

Hoffmann, Marta; Gogola-Mruk, Justyna; Kotula–Balak, Małgorzata; Ptak, Anna

doi:10.1016/j.tiv.2017.08.009

Cited by 18 publications

(9 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…lower than the 2 nM detection limit, and 43.6-102.5 nM BPS-g detected in follicular fluids of ewes in the present study), this effect on estradiol was still observed after chronic exposure, corresponding to human exposure ( 6 , 56 ). This effect is in accordance with the reported estrogenomimetic effect of bisphenols and their ability to bind to nuclear as well as membrane estrogen receptors, reported in ovarian and breast cell lines ( 9 , 57 – 59 ). The increase in estradiol secretion observed in the preovulatory follicular fluid could be related to an increase in the expression and activity of aromatase (CYP19A1) in the ovary, or a reduction in its hepatic catabolism.…”

Section: Discussionsupporting

confidence: 92%

Bisphenol S Alters the Steroidome in the Preovulatory Follicle, Oviduct Fluid and Plasma in Ewes With Contrasted Metabolic Status

et al. 2022

View full text Add to dashboard Cite

Bisphenol A (BPA), a plasticizer and endocrine disruptor, has been substituted by bisphenol S (BPS), a structural analogue that had already shown adverse effects on granulosa cell steroidogenesis. The objective of this study was to assess the effect of chronic exposure to BPS, a possible endocrine disruptor, on steroid hormones in the ovary, oviduct and plasma using the ewe as a model. Given the interaction between steroidogenesis and the metabolic status, the BPS effect was tested according to two diet groups. Eighty adult ewes were allotted to restricted (R) and well-fed (WF) groups, that were further subdivided into two subgroups. Ewes were exposed to 50 µg BPS/kg/day in their diet (R50 and WF50 groups) or were unexposed controls (R0 and WF0 groups). After at least 3 months of BPS exposure, preovulatory follicular fluid, oviduct fluid and plasma were collected and steroid hormones were analyzed by gas chromatography coupled with tandem mass spectrometry (GC-MS/MS). A deleterious effect of restricted diet on the volume of oviduct fluid and numbers of pre-ovulatory follicles was observed. Exposure to BPS impaired estradiol concentrations in both follicular and oviduct fluids of well-fed ewes and progesterone, estradiol and estrone concentrations in plasma of restricted ewes. In addition, a significant interaction between metabolic status and BPS exposure was observed for seven steroids, including estradiol. In conclusion, BPS acts in ewes as an endocrine disruptor with differential actions according to metabolic status.

show abstract

Section: Discussionsupporting

confidence: 92%

Bisphenol S Alters the Steroidome in the Preovulatory Follicle, Oviduct Fluid and Plasma in Ewes With Contrasted Metabolic Status

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Bisphenol A and tetrabromobisphenol A, two exogenous GPER ligands, have been reported to stimulate proliferation of OVCAR-3 and KGN cells (28). In the Caov-3 cell line, G-1 promotes this same cellular event through activation of the GPER/EGFR/Akt signaling pathway (20).…”

Section: Ovarian Cancermentioning

confidence: 99%

Expression and Role of the G Protein-Coupled Estrogen Receptor (GPR30/GPER) in the Development and Immune Response in Female Reproductive Cancers

2020

View full text Add to dashboard Cite

Cancer is a major public health issue and represents the second leading cause of death in women worldwide, as female reproductive-related neoplasms are the main cause of incidence and mortality. Female reproductive cancers have a close relationship to estrogens, the principal female sex steroid hormones. Estrogens exert their actions by the nuclear estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). ERα, and ERβ act as transcription factors mediating genomic effects. Besides, the G protein-coupled estrogen receptor (GPER, formerly known as GPR30) was recently described as a seven-transmembrane receptor that mediates non-genomic estrogenic signaling, including calcium mobilization, cAMP synthesis, cleavage of matrix metalloproteinases, transactivation of epidermal growth factor receptor (EGFR), and the subsequent activation of PI3K and MAPK signaling pathways, which are the reasons why it is related to cellular processes, such as cell-cycle progression, cellular proliferation, differentiation, apoptosis, migration, and invasion. Since its discovery, selective agonists and antagonists have been found and developed. GPER has been implicated in a variety of hormone-responsiveness tumors, such as breast, endometrial, ovarian, cervical, prostate, and testicular cancer as well as lung, hepatic, thyroid, colorectal, and adrenocortical cancers. Nevertheless, GPER actions in cancer are still debatable due to the conflicting information that has been reported to date, since many reports indicate that activation of this receptor can modulate carcinogenesis. In contrast, many others show that its activation inhibits tumor activity. Besides, estrogens play an essential role in the regulation of the immune system, but little information exists about the role of GPER activation on its modulation within cancer context. This review focuses on the role that the stimulation of GPER plays in female reproductive neoplasms, specifically breast, endometrial, ovarian, and cervical cancers, in its tumor activity and immune response regulation.

show abstract

“…Some compounds were also investigated taking into consideration non-classical estrogenic pathways. Hoffmann et al showed that tetrabromobisphenol A (TBBPA) stimulates the proliferation of OVCAR3 and KGN cells via the GPR30 pathway [50]. The addition of a GPER1 antagonist reversed this effect [50].…”

Section: Interaction Of Environmental Chemicals Estrogen Receptors An...mentioning

confidence: 99%

Estrogens, Estrogen Receptors and Tumor Microenvironment in Ovarian Cancer

Kozieł,

Piastowska-Ciesielska

2023

IJMS

View full text Add to dashboard Cite

Ovarian cancer is one of the most common cancers in women and the most concerning issues in gynecological oncology in recent years. It is postulated that many factors may contribute to the development of ovarian cancer, including hormonal imbalance. Estrogens are a group of hormones that have an important role both in physiological and pathological processes. In ovarian cancer, they may regulate proliferation, invasiveness and epithelial to mesenchymal transition. Estrogen signaling also takes part in the regulation of the biology of the tumor microenvironment. This review summarizes the information connected with estrogen receptors, estrogens and their association with a tumor microenvironment. Moreover, this review also includes information about the changes in estrogen receptor expression upon exposition to various environmental chemicals.

show abstract

Stimulation of ovarian cell proliferation by tetrabromobisphenol A but not tetrachlorobisphenol A through G protein-coupled receptor 30

Cited by 18 publications

References 43 publications

Bisphenol S Alters the Steroidome in the Preovulatory Follicle, Oviduct Fluid and Plasma in Ewes With Contrasted Metabolic Status

Bisphenol S Alters the Steroidome in the Preovulatory Follicle, Oviduct Fluid and Plasma in Ewes With Contrasted Metabolic Status

Expression and Role of the G Protein-Coupled Estrogen Receptor (GPR30/GPER) in the Development and Immune Response in Female Reproductive Cancers

Estrogens, Estrogen Receptors and Tumor Microenvironment in Ovarian Cancer

Contact Info

Product

Resources

About