Abstract
Paclitaxel is one of the chemotherapeutic agents frequently used in the treatment of various cancers. Paclitaxel works by promoting assembly of microtubules and stabilizing them, prventing depolymerzation. This inability to depolymerize microtubules prevents cellular replication. In this study, we used rabbit articular chondrocytes as models to determine whether paclitaxel-induced G2/M arrest might be associated with cell cycle related proteins. In chondrocytes during paclitaxel treatment, normally flat cells became rounded and in shape. Flow cytometry analysis revealed that paclitaxel accumulate cells in the G2/M phase of the cell cycle. To further cell cycle delay is mediated by mitotic cell cycle related proteins that include Cyclin B, Cdc2, Rb. Taken together, paclitaxel induced cell cycle delay. Paclitaxel-mediated mitotic arrest is associated with the modulation of cell cycle related proteins expression. Also we next investigated the effects of paclitaxel on dedifferentiation and cyclooxygenase-2 (COX-2) expression in rabbit articular chondrocytes. Immunohistochemistry and immunofluorescene study revealed that paclitaxel caused a induced dedifferentiation and suppressed COX-2 expression. Furthermore, paclitaxel enhanced prostaglandin E2 synthesis dependent of time course but independent of concentration. Thus, our data suggest that paclitaxel contributes to the expression of COX-2 and dedifferentiation in articular chondrocytes.
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