The period of mitotic arrest controls subsequent DNA damage signalling Biology Diagrams However, cells undergoing mitotic arrest eventually become committed to different fates (Fig. 2): (1) apoptosis, (SASP), which promotes chemotherapy side effects and cancer relapse [118]. In addition, senescent cancer cells can activate several pro-survival signaling pathways to become resistant to apoptosis [1, 16, 59]. If the damage is extensive, tumor suppressor pathways such as p53 mediate cell cycle arrest and apoptosis. The combination of these drugs enhances overall cytotoxicity while reducing the likelihood of resistance. Cancer cells that evade docetaxel-induced mitotic arrest can still be targeted by cyclophosphamide's DNA-damaging effects.
Disrupted passage through mitosis often leads to chromosome missegregation and the production of aneuploid progeny. Aneuploidy has long been recognized as a frequent characteristic of cancer cells and a possible cause of tumorigenesis. Drugs that target mitotic spindle assembly are frequently used to treat various types of human tumors. These lead to chronic mitotic arrest from sustained Subsequently, cells undergo mitotic arrest and since the compound disrupts spindle formation and chromosome orientation, One mechanism developed by tumor cells, when exposed to chemotherapy including antimitotic drugs in vitro, is the membrane efflux pumps of the ATP-binding cassette (ABC) family .
Human Cancer Cells Commonly Acquire DNA Damage during Mitotic Arrest Biology Diagrams
These lead to chronic mitotic arrest from sustained activation of the mitotic checkpoint. Here, we review the linkage between the mitotic checkpoint, aneuploidy, adaptation from mitotic arrest, and antimitotic drug-induced cell death. both in driving tumorigenesis and, possibly, by promoting resistance to chemotherapy. New insights that
Moreover, this consequence may have clinical implications: given the variable degree of γ-H2AX formed on drug-induced arrest in different cancer cell lines, it is plausible that the sensitivity of a tumor to antimitotic chemotherapy could be influenced by its propensity to sustain DNA damage during mitotic arrest. Tumors can be intrinsically resistant to chemotherapy before treatment or acquire resistance during treatment as a result of microevolutionary pressure on tumor cells. It is possible that prolonged mitotic arrest is responsible for ceramide elevation by paclitaxel and that any inhibition of this arrest would suppress ceramide generation and
Decoding the links between mitosis, cancer, and chemotherapy: The ... Biology Diagrams
Decoding the links between mitosis, cancer, and chemotherapy: The mitotic checkpoint, adaptation, and cell death Cancer Cell. 2005 Jul;8(1):7-12. doi: 10.1016/j.ccr.2005.06.011. These lead to chronic mitotic arrest from sustained activation of the mitotic checkpoint. Here, we review the linkage between the mitotic checkpoint, aneuploidy
