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Why mitotic cells are more sensitive to radiation therapy? 


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Mitotic cells exhibit heightened sensitivity to radiation therapy due to various mechanisms. Studies suggest that radiation induces mitotic chromosome segregation errors, leading to long-lasting aneuploidy and micronuclei formation, amplifying genome damage in cancer cells . Additionally, cancer cells resist irradiation by inducing regulated DNA breaks to prevent premature mitotic entry . Furthermore, microtubule-targeting agents like mebendazole sensitize interphase cancer cells to radiation by interfering with DNA damage response protein trafficking, independent of mitotic arrest induction . Targeting SP1, involved in tumor maintenance, with mithramycin A enhances radiation sensitivity in tumor cells by promoting mitotic catastrophe and suppressing cell death-related gene transcription . These combined factors contribute to the increased vulnerability of mitotic cells to radiation therapy.

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Mitotic cells are more sensitive to radiation therapy due to enhanced mitotic catastrophe resulting from DNA damage, which is further potentiated by Mithramycin A targeting SP1.
Mitotic cells are more sensitive to radiation therapy because cancer cells induce delayed DNA breaks to resist radiation, preventing premature mitotic entry and enhancing the effectiveness of radiation treatment.
Mitotic cells are more sensitive to radiation therapy due to induced chromosomal instability, leading to micronuclei formation and subsequent chromosomal pulverization, amplifying genome damage and reducing cell viability.
Mitotic cells are more sensitive to radiation therapy due to PSMC3IP and MND1 depletion causing ionizing radiation sensitivity, impaired DNA repair, toxic RAD51 foci accumulation, and PARP inhibitor sensitivity.
Mitotic cells are traditionally thought to be more sensitive to radiation due to DNA damage vulnerability. However, recent research suggests microtubule-targeting agents sensitize cancer cells to radiation independently of mitotic effects.

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What triggers mitosis to start?5 answersMitosis is triggered by the activation of cyclin B-cdc2 kinase. This kinase, also known as maturation promoting factor (MPF), induces the early events of mitosis, such as chromatin condensation and nuclear envelope breakdown. MPF activity leads to the hyperphosphorylation of major structural proteins of the nuclear lamina, lamins A and C, which precedes the disassembly of the nuclear lamina and triggers nuclear envelope breakdown. Additionally, calcium signals have been implicated in triggering mitosis entry and exit. Calcium oscillations are a characteristic feature of the mitotic state and may serve as a universal mitotic signal. Overall, the activation of cyclin B-cdc2 kinase and the involvement of calcium signals play crucial roles in triggering the onset of mitosis.
Is cell migration associated with mitosis?5 answersCell migration is associated with mitosis. Recent studies have shown that cell migration-induced traction forces play a role in daughter cell separation during cytokinesis. Additionally, interkinetic nuclear migration, the movement of nuclei towards the apical surface of dividing epithelial cells, is mechanically regulated and relies on a balance of forces between the mitotic cell and the surrounding tissue. The migration and invasion inhibitory protein (MIIP) has been found to regulate both cell migration and mitosis, suggesting a link between the two processes. Furthermore, research has demonstrated that cell migration can occur in the absence of mitotic activity, indicating that mitotic pressure is not the sole driving force behind cell migration. Studies have also shown that mitosis is not required for initial post-wounding migration, further supporting the idea that migration can occur independently of mitosis.
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