Mitosis and apoptosis: how is the balance set?
Anti-mitotic agents are used extensively during cancer chemotherapy. These agents target microtubules and thus block mitotic progression by activating the spindle assembly checkpoint. Following a prolonged mitotic arrest, cells either die in mitosis via apoptosis, or exit mitosis without dividing an...
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Veröffentlicht in: | Current opinion in cell biology 2013-12, Vol.25 (6), p.780-785 |
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description | Anti-mitotic agents are used extensively during cancer chemotherapy. These agents target microtubules and thus block mitotic progression by activating the spindle assembly checkpoint. Following a prolonged mitotic arrest, cells either die in mitosis via apoptosis, or exit mitosis without dividing and survive, a process known as slippage. What dictates the balance between these two fates is unclear, but recent advances highlight the importance of the pro-survival Bcl2 family, with Mcl1 degradation emerging as a key determinant of mitotic cell fate. Here we review these advances, with a view towards identifying how the balance between apoptosis and slippage can be tipped in favour of death. This in turn may open up new opportunities to sensitize cancer cells to anti-mitotic agents. |
doi_str_mv | 10.1016/j.ceb.2013.07.003 |
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These agents target microtubules and thus block mitotic progression by activating the spindle assembly checkpoint. Following a prolonged mitotic arrest, cells either die in mitosis via apoptosis, or exit mitosis without dividing and survive, a process known as slippage. What dictates the balance between these two fates is unclear, but recent advances highlight the importance of the pro-survival Bcl2 family, with Mcl1 degradation emerging as a key determinant of mitotic cell fate. Here we review these advances, with a view towards identifying how the balance between apoptosis and slippage can be tipped in favour of death. 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These agents target microtubules and thus block mitotic progression by activating the spindle assembly checkpoint. Following a prolonged mitotic arrest, cells either die in mitosis via apoptosis, or exit mitosis without dividing and survive, a process known as slippage. What dictates the balance between these two fates is unclear, but recent advances highlight the importance of the pro-survival Bcl2 family, with Mcl1 degradation emerging as a key determinant of mitotic cell fate. Here we review these advances, with a view towards identifying how the balance between apoptosis and slippage can be tipped in favour of death. 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subjects | Antimitotic Agents - pharmacology Antimitotic Agents - therapeutic use Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis - drug effects Apoptosis - physiology Apoptosis Regulatory Proteins - metabolism Bcl-2-Like Protein 11 bcl-X Protein - metabolism BH3 Interacting Domain Death Agonist Protein - metabolism Humans Internal Medicine Membrane Proteins - metabolism Microtubules - drug effects Microtubules - metabolism Mitosis - drug effects Mitosis - physiology Models, Biological Myeloid Cell Leukemia Sequence 1 Protein - metabolism Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism |
title | Mitosis and apoptosis: how is the balance set? |
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