Arsenic trioxide promotes ERK1/2-mediated phosphorylation and degradation of BIM to attenuate apoptosis in BEAS-2B cells.

Inorganic arsenic is highly toxic, widely distributed in the human environment and may result in multisystem diseases and several types of cancers. The BCL-2-interacting mediator of cell death protein (BIM) is a key modulator of the intrinsic apoptosis pathway. Interestingly, in the present study, we found that arsenic trioxide (AsO) decreased BIM levels in human bronchial epithelial cell line BEAS-2B and increased BIM levels in human lung carcinoma cell line A549 and mouse Sertoli cell line TM4.