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KMID : 1140120110160040379
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Cancer Prevention Research
2011 Volume.16 No. 4 p.379 ~ p.386
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Effects of RKIP Level & Sensitivity of Chemotherapy Agent, Paclitaxel (TAXOL) on Pancreatic Cancer Cell Lines
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Kim Sung-Ok
Kim Mi-kyung
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Abstract
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To test our hypothesis that RKIP induction using a Histone Deacetylase Inhibitor, Trichostatin A (TSA) can increase cancer cell sensitivity we treated pancreatic cancer cells with/without the Paclitaxel (TAXOL), a chemotheraphy agent, for 24h and recorded the cell growth and viability. We then repeated the experiment using a combination of TSA plus TAXOL and compared these results with those from treatment with TAXOL alone. The other hands, to confirm whether RKIP knock-out influences inversely in cancer cell death. We followed this experiment with an RKIP Western blot to quantify the RKIP levels in the TSA treated cell lines in order to determine what role RKIP induction played in cell death. By proving that RKIP induction via histion deacetylase inhibition was directly related to decreased drug resistance. And also knock-out RKIP showed inversely results. We hope to aid in the progress towards a novel therapeutic approach to treating pancreatic cancer in which RKIP levels, and thus cancer cell sensitivity, can be modulated. By assessing patient RKIP levels before chemotherapy, doctors will be able to determine how sensitive a patient’s cells are to particular chemotherapeutic agents at particular concentrations and develop a personalized treatment that will be the most effective for that patient.
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KEYWORD
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RKIP, Trichonstatin a, Paclitaxel (TAXOL), Pancreatic cancer cells
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