Low doses of bisphenol A stimulate the proliferation of breast cancer cells via ERK1/2/ERRγ signals

Song, Haixing; Zhang, Tao; Yang, Ping; Li, Min-Hui; Yang, Yuhan; Wang, Yuanyuan; Du, Jie; Pan, Kehou; Zhang, Kun

doi:10.1016/j.tiv.2015.09.009

Cited by 95 publications

(74 citation statements)

References 48 publications

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“…Otherwise, high-dose BPA inhibited proliferation, even showed slight cell toxicity in the highest concentration (10 μM BPA). The highest cell viability (132.4%, P<0.01) was achieved in 10 nM BPA treatment, which was consistent with results of Song et al [11] . In addition, another study found that the estrogenic activity of BPA increased via a dose-dependent manner in HeLa cells, and the most effective concentration is 1 μM (P<0.01) [12] , which indicated that estrogenic effect of BPA varied with different cells.…”

Section: Resultssupporting

confidence: 91%

Estrogenic Joint Effect of BPA and DES on MCF-7 Cells

Pu¹,

Ma²,

Xu³

et al. 2016

Proceedings of the 2016 5th International Conference on Advanced Materials and Computer Science

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Abstract.Nowadays environmental health problems caused by Endocrine disrupting chemicals (EDCs) really attracted much concern. Bisphenol A (BPA) and diethylstilbestrol (DES), synthetic estrogens that have similar structure, were proved to be related to various type of cancers, including breast cancer. In this paper, cell viability assay was used as evaluation basis to examine the estrogenic effect and joint effect of BPA, DES and 17β-estradiol (E2). The result showed that the proliferation of MCF-7 cells was promoted by environmental relevant doses of BPA and DES. And the more intense effect would be realized when combining BPA with DES. In addition, BPA or DES could strengthen the estrogenic effect of E2. However, for ternary mixture of E2, BPA and DES, all the experimental groups performed an antagonism.

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Section: Resultssupporting

confidence: 91%

Estrogenic Joint Effect of BPA and DES on MCF-7 Cells

Pu¹,

Ma²,

Xu³

et al. 2016

Proceedings of the 2016 5th International Conference on Advanced Materials and Computer Science

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“…21,22 Estrogen signals have been proven to trigger the proliferation and angiogenesis of HA cells. 32 Whether the estrogen-related receptor is also involved in In summary, the work presented here showed that nanomolar BPA can significantly trigger the migration and invasion of HA cells via induction of EMT. 30 Recently, the family of estrogen-related receptor is suggested to have very high bind affinity to BPA 31 and therefore mediates the estrogenic effects of BPA.…”

Section: Discussionmentioning

confidence: 85%

Bisphenol A regulates Snail‐mediated epithelial‐mesenchymal transition in hemangioma cells

Zhai¹,

Jiang²,

Li³

et al. 2016

Cell Biochemistry & Function

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Hemangioma (HA) can be exposed to bisphenol A (BPA) through direct skin absorption. Although numerous studies indicated that BPA can trigger the progression of cancers, there is no study concerning the effects of BPA on development of HA. Our present study revealed that nanomolar BPA can significantly increase the in vitro migration and invasion of HA cells via induction of epithelial-mesenchymal transition (EMT), which was evidenced by the upregulation of vimentin and downregulation of E-cadherin. The BPA treatment also significantly increased the expression and nuclear localization of Snail and the key transcription factor of EMT, while it had no effect on the expression of other transcription factors such as Slug, Twist, or ZEB1. Silencing of Snail by small interfering RNAs attenuated BPA-induced downregulation of cadherin and upregulation of vimentin, suggesting that Snail is essential for BPA-induced EMT. Both estrogen receptor α (ERα) and G protein-coupled estrogen receptor (GPER) were expressed in HA cells; furthermore, BPA treatment can increase the expression of both ERα and GPER. However, only the inhibitor of ERα (ICI 182, 780), and not GPER (G15), can abolish BPA-induced upregulation of Snail. It suggested that ERα is involved in BPA-induced EMT of HA cells. Collectively, our data suggested that BPA can trigger the EMT of HA cells via ERα/Snail signals. It indicated that more attention should be paid to the skin exposure to BPA for HA patients.

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“…For example, low concentrations of BPA promoted proliferation of male mouse germ cells by inducing the G protein‐coupled receptor 30 (GPR30) and oestrogen receptor (ER)‐α (Marmugi et al, ). Furthermore, low doses of BPA significantly upregulated ERK1/2/ERRγ expression and then stimulated proliferation of breast cancer cells (Song et al, ). Our recent work also revealed that BPA increased the level of 17β‐estradiol accumulation and cellular proliferation (Wu et al, ).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A attenuates thyroxine‐induced apoptosis in ovarian granulosa cells of pigs

Song

Wei

et al. 2019

Reprod Domestic Animals

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Contents Bisphenol A (BPA) is a chemical of high production volume that is used widely in many industries and is known as a xenooestrogen and anti‐thyroid hormone endocrine disrupter. There is little information regarding the effects of BPA in the presence of thyroid hormone on porcine granulosa cell development. Thus, the primary granulosa cells were treated with thyroxine (T4, 10 nM), BPA (10 µM) or T4 plus BPA; we subsequently evaluated the effects of T4 or BPA on 17β‐estradiol synthesis, cellular proliferation and apoptosis. Our data showed that BPA significantly increased the accumulation of 17β‐estradiol and promoted granulosa cell proliferation, whereas T4 significantly decreased 17β‐estradiol and had no effect on cellular proliferation. In addition, it was noteworthy that T4 treatment induced apoptosis in porcine granulosa cells and BPA co‐incubation attenuated T4‐induced apoptosis as shown from flow cytometric assay analysis. We hypothesized that BPA attenuates T4‐induced apoptosis by regulating 17β‐estradiol accumulation and oestrogen receptor‐mediated signalling pathways. In conclusion, our results demonstrated that T4 affected 17β‐estradiol accumulation and induced cellular apoptosis, but did not affect granulosa cell proliferation. Exposure to BPA increased 17β‐estradiol accumulation, promoted granulosa cell proliferation and attenuated T4‐induced apoptosis in porcine granulosa cells in vitro.

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Low doses of bisphenol A stimulate the proliferation of breast cancer cells via ERK1/2/ERRγ signals

Cited by 95 publications

References 48 publications

Estrogenic Joint Effect of BPA and DES on MCF-7 Cells

Estrogenic Joint Effect of BPA and DES on MCF-7 Cells

Bisphenol A regulates Snail‐mediated epithelial‐mesenchymal transition in hemangioma cells

Bisphenol A attenuates thyroxine‐induced apoptosis in ovarian granulosa cells of pigs

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