Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway

@article{Zhang2019EffectsOB,
  title={Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway},
  author={Qi Zhang and Shuang-hu Wu and Lu Liu and Xiaohong Hou and Jianjun Jiang and Xuetao Wei and Weidong Hao},
  journal={Journal of Applied Toxicology},
  year={2019},
  volume={39},
  pages={271 - 281}
}
Bisphenol A (BPA) is widely used as the raw material for the production of plastics and paper products. People can be exposed to BPA through dermal contact, particularly for cashiers in contact with thermal paper every day. BPA is a known endocrine disruptor that has been shown to be carcinogenic. Many tumors show weak gap junctional intercellular communication (GJIC) function. The aim of this study was to investigate the effects and possible mechanisms of BPA's action on GJIC of human HaCaT… 
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References

SHOWING 1-10 OF 77 REFERENCES
Inhibitory effect of Bisphenol A on gap junctional intercellular communication in an epithelial cell line of rat mammary tissue
TLDR
The results suggest that BPA inhibits GJIC through a modulation of the gating of gap junction channels, not through a genomic modulation of Cx43.
Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals
TLDR
Laccase appears to impair BPA action(s), representing an invaluable bioremediation enzyme that participates to BPA‐induced cytotoxicity.
Effects of bisphenol A on the proliferation and cell cycle of HBL-100 cells.
Bisphenol A regulates Snail‐mediated epithelial‐mesenchymal transition in hemangioma cells
TLDR
It is 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.
Bisphenol A interacts with the estrogen receptor α in a distinct manner from estradiol
Treatment with bisphenol A and methoxychlor results in the growth of human breast cancer cells and alteration of the expression of cell cycle-related genes, cyclin D1 and p21, via an estrogen receptor-dependent signaling pathway.
TLDR
Results confirmed the carcinogenicity of EDCs in vitro and induced the cancer cell proliferation by the upregulation of genes that promote the cell cycle and the downregulation of anti-proliferative genes.
Green tea prevents down-regulation of gap junction intercellular communication in human keratinocytes treated with PMA
TLDR
An important role of GJIC played in carcinogenesis involving human keratinocytes and green tea as a useful anticancer diet is suggested and EC and EGCG inhibited its effect.
Oral Exposure to Bisphenol A Increases Dimethylbenzanthracene-Induced Mammary Cancer in Rats
TLDR
Evidence is provided that maternal exposure to BPA during lactation increases mammary carcinogenesis in a DMBA-induced model of rodent mammary cancer, and changes in PR-A, SRC 1–3, erbB3, and Akt activity are consistent with increased cell proliferation and decreased apoptosis playing a role in mammarycancer susceptibility.
A review of the carcinogenic potential of bisphenol A.
Silver nanoparticles increase connexin43‐mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen‐activated protein kinase signal pathway
TLDR
Results revealed that non‐coated AgNP exposure at subcytotoxic doses increase GJIC partially via Cx43 upregulation, and new insight is provided into the potential mechanism of AgNP biological activity.
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