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Benzyl isothiocyanate-mediated generation of reactive oxygen species causes cell cycle arrest and induces apoptosis via activation of MAPK in human pancreatic cancer cells
Carcinogenesis, 10/08/09

Sahu RP et al. – NAC or tiron prevented G2/M arrest by blocking G2/M regulatory proteins and completely protected the cells from BITC–induced apoptosis. Taken together, the results suggest that BITC–mediated G2/M arrest is mediated through ERK activation, whereas apoptosis is via ERK, JNK and P38.

Exclusive Author Commentary
Sanjay K. Srivastava, Ph.D., 10/08/09

Epidemilogical and case controlled studies support the notion that consumption cruciferous vegetables reduces the risk of pancreatic cancer. Benzyl isothiocyanate (BITC) is the active ingredient present in these vegetables. We have shown that BITC treatment suppress the growth of human pancreatic cancer cells without affecting the viability of normal pancreatic epithelial cells. Orally feeding BITC suppress the growth of implanted pancreatic tumors in mice by inducing cell death in tumor cells. We demonstrated that BITC treatment inhibits STAT-3, an oncogene overexpressed in various tumors including pancreatic (Sahu and Srivastava, JNCI, 101, 176-193, 2009). Taken together, several signaling proteins, which are deregulated in cancer are modulated by BITC leading to tumor growth suppression. Detailed studies are in progress.

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