Arsenic is a human environmental carcinogen that causes lung, skin, and bladder cancers.  Innumerable genes and gene products, which are critical in the regulation of numerous cellular functions, are involved in the complex, multistage process of carcinogenesis. Thus, the elucidation of molecular and cellular targets critical in cancer development and prevention is an area of intensive research attention. The prevailing idea today is that cancer may be prevented or treated by targeting specific cancer genes, signaling proteins, and transcription factors. In particular, the mitogen-activated protein (MAP) kinase signaling pathways are activated to different degrees by various tumor promoters. Their activation can result in a multitude of cellular responses including apoptosis, proliferation, inflammation, differentiation, and development. Over the last few years, our laboratory has shown arsenic induced activation of various distinct kinases and their target substrates. These protein kinases exhibit a distinctive activity or higher expression in cancer tissues compared to normal tissues; and therefore might be excellent targets for chemopreventive agents. These proteins include MSK1, RSK1, p38, Erk, vimentin, glucose-regulated protein 78 (GRP78), insulin-like growth factor receptor 1 (IGF-1R), paxillin, T-LAK cell-originated protein kinase (TOPK), c-Jun N-terminal kinase 2, and the zeta chain associated protein of 70 kDa (ZAP-70). We found these signals play a critical role in neoplastic cell transformation and can be used as targets for cancer prevention.

Arsenic induced signal transduction in carcinogenesis and as targets for cancer prevention

246th National Meeting (2013)

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