Paclitaxel is a novel anti-microtubule drug, through promoting tubulin polymerization, inhibiting depolymerization, remain tubulin stable, inhibit cell mitosis.
Vitro experiments show that paclitaxel has significant radiosensitizing effect, may be suspending the cells in G2 and M phase of radiotherapy sensitive.
Paclitaxel belongs to mitotic inhibitors or spindle toxins, have a different mechanism of action with currently used chemotherapy drugs, it is the assembly to induce and promote microtubule. Taxol has polymerization and stabilizing microtubule role, resulting in rapidly dividing tumor cells firmly fixed during mitosis phase, make the cancer cells replication was blocking and death.
Microtubules are a component of the eukaryotic cell, which is composed of two similar polypeptides (a and p) microtubule subunits dimer. Under normal circumstances, microtubules and tubulin dimer exists dynamic balance. Paclitaxel is a kind of pharmaceutical raw materials can make them lose this dynamic balance, induce and promote tubulin polymerization, preventing depolymerization, stable microtubules. These effects lead to cells during mitosis cannot form a spindle and spindle fibers, inhibit cell division and proliferation, thus play an anti-tumor effect.
In vitro studies shown that paclitaxel concentration was dependent, reversibly bound to microtubules, in particular binding to N-terminal the P- tubulin subunits, this effect reduces the microtubule protein concentration of polymerization required, make the dynamic equilibrium towards the direction of microtubule assembly, increasing the rate of microtubule polymerization and yield. Paclitaxel-induced microtubule formation is shorter, and about ten times larger than not use paclitaxel’s normal buckling microtubules. Paclitaxel in the ratio of 1:1 binding to microtubules, indicated that drugs in microtubule only have one binding site. In addition, the microtubule network required by paclitaxel inhibited mitosis normal dynamic regeneration, preventing the normal mitotic spindle formation, resulting in chromosome breakage, and inhibiting cell replication. Paclitaxel and cholesterol and A2780 ovarian cancer cell lines incubated 24h, 99% cell death, of which 57% cells enter division stage, and occurs a wide range of nuclear damage.
Taxol changes cells mitosis process, make the mitotic duration from 0.5h to 15h, and inhibit cytokinesis, leading to form multinucleate cells. These multinucleate cells continue to revert to division stage, and then tried to divide again, but there are not arresting cells, in many cells also observed micronuclei. Inhibit spindle forming seems related to this abnormal mitosis. Low concentrations of paclitaxel in vitro (less than 8.5pg/L) block metaphase transitions to anaphase in cell cycle, prevent cell proliferation, without increasing the amount of microtubule multimer or form microtubule spindle. Paclitaxel inhibits cell proliferation and block cell metaphase degree parallel. Higher concentration paclitaxel (greater than 8.5fig/L) increased microtubule polymer amount, in 282pg/L, it is 500% higher than the control level, resulting in forming large spindle of microtubules. Leukemia cells and 85pg/L or greater concentrations paclitaxel incubated for 24h, 40% of the cell contraction, chromosome concentrated.
Article Source:http://www.cospcn.com
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