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- W3157753208 abstract "The ruthenium-based drug imidazolium trans-imidazoledimethlysulfoxide-tetrachlororuthenate (NAMI-A) has previously demonstrated anti-proliferative and anti-metastatic effects, in addition to limited cellular and host toxicity. The goal of this study was to evaluate effects of NAMI-A on rat intestinal epithelial (RIE-1) cells transformed by K-Ras 12V. A K-Ras 12V genetic mutation causes the Ras GTPase to be chronically activated, leading to unregulated cell cycle progression, altered morphology, and other cancer cell phenotypes. RIE-1 cells were treated with NAMI-A, and effects on cytotoxicity, proliferation, anchorage-independent growth, invasion, morphology, and signal transduction downstream of Ras were investigated. NAMI-A, at concentrations up to 200 #956;M, was nontoxic to RIE-1 cells, and NAMI-A selectively reduced anchorage-independent proliferation and inhibited Matrigel invasion of Ras-transformed cells. Exposure of either nontransformed or Ras-transformed cells to NAMI-A for up to twenty-four hours did not alter cell morphology. Finally, western analysis was used to examine activation of ERK (extracellular-regulated protein kinase) and Akt kinase, effector pathways downstream of Ras and involved in progression and maintenance of the transformed state. NAMI-A treatment caused an upregulation of both ERK and Akt activation, as shown by an increase in phosphorylation, in nontransformed cells and caused a slight downregulation of Akt activation in Ras-transformed cells. Given that the anti-proliferative and anti-metastatic effects of NAMI-A on RIE-1 cells have been previously shown to be selective towards the Ras-transformed cells, this study proposed an interesting shift to the potential effects of NAMI-A on molecular pathways downstream of Ras in nontransformed cells. Taken together, our studies indicate that NAMI-A exhibits anticancer effects in Ras-transformed cells and upregulates ERK and Akt activation in nontransformed cells. These studies provide novel evidence of the selective anticancer effects of NAMI-A in Ras-transformed RIE-1 cells as well as novel effects of NAMI-A on Akt, suggesting that NAMI-A could target other proteins that lie upstream of both ERK and Akt signaling. Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4625." @default.
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- W3157753208 date "2009-05-01" @default.
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- W3157753208 title "Abstract #4625: Effect of NAMI-A on K-Ras-mediated oncogenic transformation and signal transduction" @default.
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