Does Taxol induce apoptosis?
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Does Taxol induce apoptosis?
Taxol-induced apoptosis is mediated by the ERK and p38 MAPK cascades in MCF7 cell and Taxol upregulates certain cell cycle proteins. Treatment of MCF7 cells with 50 ng/ml of Taxol for 1–2 days induces massive apoptosis in MCF7 cells.
How does Taxol cause apoptosis?
The anticancer agent, taxol, stabilizes tubulin polymerization, resulting in arrest at the G2/M phase of the cell cycle and apoptotic cell death.
What does Taxol do to the cell cycle?
Taxol is an anti-mitotic agent that binds to microtubules and stabilizes them against depolymerization; therefore, Taxol inhibits cell replication by disrupting normal mitotic spindle formation and arresting cell growth in the M phase of the cell cycle [12-14].
How does Taxol cause mitotic arrest?
Taxol induces two forms of cell cycle arrest, which in turn induce two independent apoptotic pathways. Arrest in prophase induces rapid onset of a p53-independent pathway, whereas G1-block and the resulting slow (3–5 days) apoptotic pathway are p53 dependent.
Which phase of the cell cycle is affected by paclitaxel?
Paclitaxel inhibits progression of mitotic cells to G1 phase by interference with spindle formation without affecting other microtubule functions during anaphase and telephase. Cancer Res.
How does Taxol chemo work?
Taxol, an antimitotic agent used to treat cancer, blocks cancer cell growth by stopping cell division, resulting in cell death. An NCI-funded clinical trial found that 30 percent of patients with advanced ovarian cancer responded positively to Taxol treatment.
What is the mechanism of action of Taxol?
Mechanism of action of paclitaxel. Paclitaxel targets microtubules. At high concentration, PTX causes mitotic arrest at G2/M phase whereas at low concentration, apoptosis is induced at G0 and G1/S phase either via Raf-1 kinase activation or p53/p21 depending on the dose concentration.
How does paclitaxel affect cells in G2 phase?
We found that the first paclitaxel treatment synchronized the cells at the G2/M phase but releasing the block by stopping the treatment allowed a large number of cells to enter the next cell-cycle by a synchronized manner.
