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Colchicine and paclitaxel initiate apoptosis in IAR 20 rat hepatocytes through SAPK/JNK and caspase-3 activation via time dependent and p53 independent mechanisms

Colchicine and paclitaxel are two common drugs used in chemotherapy to halt tumor growth. In the present study IAR 20 cells were treated for 24 and 48 hr with colchicine and paclitaxel alone, in combination or no drug which served as a control. Through the use of Western blotting, we determined that the treatments affected expression due of several proteins including bcl-2, bax, p53 and caspase-8. The changes observed in protein expression due to the treatments correlated to the photomicrographs of the cells in culture and cell viability, indicating that the drugs were activating and initiating apoptosis. Interestingly, morphological changes such as membrane blebbing and cell swelling (indicators of apoptosis) were observed in the treated cultures and even more important the combined treatment yielded both changes in morphology. Also, activity assays were performed to study the effects the treatments had on the activities of SAPK/JNK and caspase-3, known activators of apoptosis. High activities of SAPK/JNK and caspase-3 in 48 hr treatments directly influenced cell viability in that the treatments with the highest activities yielded the lowest cell numbers, indicating that apoptosis was occurring. Based on these findings it was concluded that combined treatments of colchicine and paclitaxel are not advantageous in hepatocytes and could provide some insight into the treatment of liver cancer. Additionally, it appeared the drugs were initiating apoptosis in a p53 independent manner. / Department of Biology

Identiferoai:union.ndltd.org:BSU/oai:cardinalscholar.bsu.edu:handle/187259
Date January 2002
CreatorsBlosser, Wayne D.
ContributorsOlesen, James B.
Source SetsBall State University
Detected LanguageEnglish
Formatv, 56 leaves : ill. (some col.) ; 28 cm.
SourceVirtual Press

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