Targeting microtubules for cancer therapy Sample Clauses

Targeting microtubules for cancer therapy. Agents that disrupt the microtubule cytoskeleton are probably the most effective class of chemotherapeutics to date (136). Initially, the essentialness of microtubules in cell division was the basis of the development for new generation of MTAs since the strategy was to inhibit cell division. Now, the success of MTAs is also attributed to the grave importance of this cytoskeletal protein in the maintenance of cell shape and polarity, intracellular transport and signal transduction. This has been validated by the extensive research into the mechanism of clinically successful MTAs including taxanes and the vinca alkaloids. Much attention has been given to the discovery of agents that also act to disrupt microtubules with a majority of these being natural products or compounds derived from them (137). Due to this, the MTAs represent one of the most diverse classes of molecules compared to other classes of anticancer agents. Drug binding sites Upon binding to tubulin, microtubule-targeting agents are known to block cell division. This activity leads to the accumulation of cells in the G2/M phase of the cell cycle and ultimately mitotic arrest. Due the ability of these agents to inhibit cell division, these agents are often referred to as anti-mitotics. MTAs disrupt the microtubule network by both inducing microtubule polymerization through stabilizing microtubules and increasing the microtubule polymer mass or by inhibiting microtubule assembly. Though these activities are distinctly different, both induce mitotic arrest and apoptotic cell death. Interestingly, the three well established drug binding sites for MTAs on tubulin all lie on the β-tubulin subunit. These sites include the taxane, vinca alkaloid, and colchicine binding sites. Recently, other sites on tubulin have been proposed though the validity of these findings is currently under investigation (Fig. 1.12).
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