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| Mitotic arrest is a cell-cycle state in which a cell is prevented from completing mitosis, usually because the spindle-assembly checkpoint detects improper chromosome alignment, defective kinetochore attachment, spindle damage, or incomplete chromosome segregation. Mitotic arrest commonly occurs during metaphase and is associated with sustained cyclin B1/CDK1 activity, checkpoint proteins such as MAD2, BUB1, BUBR1, and MPS1, and inhibition of the anaphase-promoting complex/cyclosome (APC/C). In cancer cells, prolonged mitotic arrest may suppress tumour growth by preventing cell division and can lead to apoptosis, mitotic catastrophe, senescence, or abnormal exit from mitosis. Compounds that disrupt microtubules, centrosomes, kinetochores, or spindle-checkpoint signalling frequently induce mitotic arrest. However, some cells escape through mitotic slippage, which may produce polyploid or genetically unstable surviving cells. Generally favourable anticancer direction: increased or prolonged mitotic arrest in tumour cells, particularly when followed by apoptosis or mitotic catastrophe. The effect should be interpreted cautiously if the study also reports mitotic slippage, polyploidy, or survival of genomically unstable cells. |
| 6690- | DFC, | Diclofenac: A Nonsteroidal Anti-Inflammatory Drug Inducing Cancer Cell Death by Inhibiting Microtubule Polymerization and Autophagy Flux |
| - | in-vitro, | Cerv, | HeLa |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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