Benzyl isothiocyanate promotes miR‐99a expression through ERK/AP‐1‐dependent pathway in bladder cancer cells

• DOI: 10.1002/tox.22841
• Publication Date: 2019-10-06T08:55:59Z
• Authors: Te‐Fu Tsai; Po‐Chun Chen; Yi‐Chia Lin; Kuang‐Yu Chou; Hung‐En Chen; Chao‐Yen Ho; Ji‐Fan Lin; Thomas I‐S. Hwang
• Keywords: Benzyl isothiocyanate; Sulforaphane

Benzyl isothiocyanate (BITC), a bioactive natural product present in cruciferous vegetables, has been proved to prevent cancer progression through various mechanisms. In our previous report, we that BITC exhibits antitumor effects bladder by suppressing IGF1R, FGFR3, and mTOR, which is mediated miR-99a expression. this study, identified the signal pathway involved regulating expression after exposure cancer. Treatment with different concentrations resulted induction of cell lines. Activation extracellular signal-regulated protein kinase (ERK) c-jun N-terminal was observed treatment for 24 hours. Interestingly, using chemical inhibitor candidate pathways, found only ERK required Furthermore, evaluated transcription factor may contribute response treatment. The results indicated c-Jun/AP-1 activated Moreover, confirmed activation immunofluorescence luciferase reporter assay. showed markedly improved nuclear translocation activity dose dependently. Finally, pretreatment U0126 diminished c-Jun phosphorylation transcriptional activation, suggesting elicits ERK/c-Jun transduction, responsible work identifies mechanism upregulation treatment, provides an explanation biological function work.