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Updated: Sep 30, 2026

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
Published on: May 14, 2018
Paclitaxel-induced FasL-independent apoptosis and slow (non-apoptotic) cell death
Mikhail V Blagosklonny1, Robert Robey, M Saeed Sheikh
1Medicine Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. M_Blagosklonny@NYMC.Edu
Abstract:
Microtubule-active drugs, including paclitaxel (Taxol, PTX), cause mitotic arrest, and this can result in apoptosis. A recently study has reported that PTX mediates apoptosis by upregulating FasL in Jurkat and MDA-231 cells. In contrast to the previous report, we found that anti-FasL antibodies failed to inhibit PTX-induced apoptosis in Jurkat cells. In MDA-231 cells, neither FasL nor PTX induced apoptosis. In these cells, PTX caused slow cell death without activation of caspase-3 or -8 or PARP cleavage. Doxorubicin at cytostatic concentrations did not affect FasL-induced apoptosis but inhibited PTX-induced apoptosis in Jurkat cells. Following PTX-induced mitotic arrest Jurkat cells undergo apoptosis, whereas MDA-MB-231 cells exit mitosis and form multinucleated cells which then die in a slower non-apoptotic manner.
Insights
Paclitaxel (PTX) causes cell death, but its mechanism differs by cell type. PTX-induced apoptosis in Jurkat cells is FasL-independent, while MDA-MB-231 cells undergo slower, non-apoptotic death after mitotic arrest.
Area of Science:
- Cell Biology
- Molecular Biology
- Pharmacology
Background:
- Microtubule-active drugs like paclitaxel (PTX) induce mitotic arrest, potentially leading to apoptosis.
- Previous studies suggested PTX mediates apoptosis via FasL upregulation in Jurkat and MDA-231 cells.
Purpose of the Study:
- To investigate the role of FasL in paclitaxel-induced apoptosis in Jurkat and MDA-231 cells.
- To elucidate the distinct mechanisms of cell death induced by PTX in different cell lines.
Main Methods:
- Treatment of Jurkat and MDA-231 cells with paclitaxel (PTX) and anti-FasL antibodies.
- Assessment of apoptosis induction, caspase activation (caspase-3, -8), and PARP cleavage.
- Evaluation of cell fate following PTX-induced mitotic arrest, including multinucleation.
Main Results:
- Anti-FasL antibodies did not inhibit PTX-induced apoptosis in Jurkat cells.
- PTX did not induce apoptosis in MDA-231 cells; instead, it caused slow cell death without caspase activation or PARP cleavage.
- Doxorubicin inhibited PTX-induced apoptosis in Jurkat cells but not FasL-induced apoptosis.
- Jurkat cells underwent apoptosis after PTX-induced mitotic arrest, while MDA-MB-231 cells formed multinucleated cells and died via a non-apoptotic pathway.
Conclusions:
- Paclitaxel-induced apoptosis in Jurkat cells is independent of the FasL pathway.
- MDA-MB-231 cells exhibit a distinct, slower, non-apoptotic cell death mechanism following PTX-induced mitotic arrest.
- Cellular response to paclitaxel varies, highlighting different cell death pathways activated by mitotic arrest.
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