bpa exposure

Chemico-Biological Interactions

Hemangioma (IHA) is the most common benign tumor in infants caused by hyperproliferation of mesoblastic vascular tissues. Studies indicated that estrogenic signals have positive roles in its progression, while potential roles of endocrine disrupting compounds (EDCs) on its development are largely unknown. Our present study found that bisphenol S (BPS), the “safety” analog of bisphenol A (BPA), can trigger proliferation of HA cells and induce G1 to S transition of cell cycle at nanomolar concentrations. Further, BPS increased the expression of basic fibroblast growth factor (bFGF) in HA cells. Knockdown of bFGF can attenuate BPS-induced proliferation of HA cells, suggesting the essential role of bFGF in BPS-induced HA development. BPS can increase the transcription and mRNA stability of bFGF, while had no effect on its mRNA export or protein stability. Mechanistically, BPS can activate p65 to initiate bFGF transcription and decrease miR-155-5p to upregulate the mRNA stability of bFGF. Collectively, our study revealed that BPS can trigger the malignancy of HA cells via induction of cell proliferation and cell cycle transition. This is due to that BPS can increase the expression of bFGF via activation of p65 and down regulation of miR-155-5p.

WITHDRAWN: Bisphenol S triggers the malignancy of hemangioma cells via regulation of basic fibroblast growth factor