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• W2017134140 abstract "Purpose: Despite recent advances in therapies, the beneficial effect unfortunately remains modest in pancreatic cancer due to a high degree of inherent and acquired chemo-resistance. We previously reported that genistein augments pancreatic tumor sensitivity to Gemcitabine and Cisplatin due to down regulation of NF-κB and Akt (Cancer Res. 2005; 65:9064-72; Cancer 2006; 106:1260-68). Further, as a proof of concept in support of our hypothesis, we investigated whether 3,3′-Diindolylmethane (DIM), an inhibitor of NF-κB could elicit similar effects on Panc-1, COLO 357, MDA Panc-28 and stably transfected MDA Panc-28/IκBαM (the MDA Panc-28/ IkBaM cells expressing phosphorylation defective IκBα [S32, 36A] that blocks NF-κB activation) pancreatic cancer cells. Method: Panc-1, COLO 357, MDA Panc-28 and MDA Panc-28/ IκBαM cells were cultured in complete DMEM media with and without DIM (0-100 μM) alone for 72 hrs. The response to multiple chemotherapeutic agents (Oxaliplatin, Gemcitabine and Cisplatin) was assessed in vitro using MTT and quantifying cytoplasmic histone-DNA fragments using Cell Death Detection ELISA kit upon pretreatment with 25-50 μM DIM (48 hrs) followed by chemotherapeutic agents for an additional 48-72 hrs. The molecular mechanism for enhanced chemosensitivity was investigated by performing Western immunobloting for pAkt, Survivin, Bcl-2, Bcl-xL, and PARP by single regimen treatment and under conditions of pretreatment with DIM. Additionally, gel shift assay was performed to elucidate whether activation of the basal NF-κB transcription factor was responsible for suppressing apoptosis and whether DIM mediated abrogation of NF-κB leads to sensitization and killing of pancreatic cancer cells by multiple chemotherapeutic agents. Results: The MDA Panc-28/ IκBαM and COLO 357 cells without NF-κB expression were found relatively more sensitive to DIM compared to parental MDA Panc-28 cells. DIM pretreatment also significantly enhanced the anti-proliferative and apoptotic effect of Oxaliplatin, Gemcitabine and Cisplatin in these cells relative to untreated control and the parental MDA Panc-28 cells. Several downstream regulatory target molecules under influence of NF-κB, such as Bcl-xL, Bcl-2, Cyclin D1, Survivin and MMP-9, were affected to different degrees under DIM pretreatment conditions. Conclusion: Our results strongly suggest that chemosensitization of human pancreatic cancer cells is, at least, due to inactivation of NF-κB and Akt signaling caused by DIM. Thus, our results provide evidence in support of rational design of pre-clinical in vivo and human studies targeting NF-κB and Akt signaling pathway by DIM, a known chemopreventive agent for better outcome of chemotherapy of pancreatic cancer." @default.
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• W2017134140 date "2006-11-01" @default.
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• W2017134140 title "MOLECULAR EVIDENCE OF 3,3???-DIINDOLYLMETHANE INDUCED ENHANCEMENT IN CHEMOSENSITIVITY OF PANCREATIC CANCER CELLS TO MULTIPLE CHEMOTHERAPEUTIC AGENTS" @default.
• W2017134140 doi "https://doi.org/10.1097/00006676-200611000-00035" @default.
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