IMR Press / FBE / Volume 1 / Issue 2 / DOI: 10.2741/E55

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Benzyl isothiocyanate sensitizes human pancreatic cancer cells to radiation therapy
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1 Department of Pharmaceutical Sciences and Cancer Biology Center, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, Texas
2 Department of Radiation Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh
Academic Editor:Sanjay K. Srivastava
Front. Biosci. (Elite Ed) 2009, 1(2), 568–576; https://doi.org/10.2741/E55
Published: 1 June 2009
(This article belongs to the Special Issue NF-kB: a potential target for cancer)
Abstract

Increase in systemic toxicity and resistance are the major drawbacks of radiation therapy in the treatment of pancreatic cancer. We have shown previously that BITC inhibits the growth of human pancreatic cancer cells and induces apoptosis. Here we determined whether BITC could sensitize BxPC-3 cells and increase the therapeutic potential of γ-irradiation. Cells were pretreated with 2.5µM BITC for 24h followed by exposure to 5 Gy of γ-irradiation and were allowed to grow for another 24 or 48h before being analyzed. Combination of BITC and γ-irradiation significantly reduced survival of cells and caused significantly enhanced arrest of cells in G2/M phase as compared to cells exposed to γ-irradiation alone. G2/M arrest was associated with DNA damage leading to the phosphorylation of ATR (Ser-428), Chk2 (Thr-68), Cdc25C (Ser-216), Cdk-1 (Tyr-15) and induction of p21Waf1/Cip1. However, combination treatment after 48h caused 2.8-fold increase in apoptosis in BxPC-3 cells. Apoptosis at 48h was associated with NF-kB inhibition and p38 activation. Taken together, results of the present study suggest that the apoptosis-inducing effect of γ-irradiation can be increased by BITC.

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