Inactivation of Mad2B Enhances Apoptosis in Human Cervical Cancer Cell Line upon Cisplatin-Induced DNA Damage
Ju Hwan Kim, Hak Rim Kim, Rajnikant Patel
Abstract
. In contrast to Mad2A, Mad2B does not localize to kinetochores or binds to Cdc20 in spindle assembly checkpoint-activated cells. Loss of the Mad2B protein leads to damaged nuclei following cisplatin-induced DNA damage. Mad2B/Rev7 depletion causes the accumulation of damaged nuclei, thereby accelerating apoptosis in human cancer cells in response to cisplatin-induced DNA damage. Therefore, our results suggest that Mad2B may be a critical modulator of DNA damage response.
Topics & Concepts
DNA damageCisplatinG2-M DNA damage checkpointMitosisCell biologyBiologyCell cycle checkpointDNA repairMolecular biologyProliferating cell nuclear antigenCell cycleChemistryApoptosisCancer researchDNABiochemistryGeneticsChemotherapyMicrotubule and mitosis dynamicsDNA Repair MechanismsNuclear Structure and Function