Role of CMT2, mitotic checkpoint regulator, in tumor cell

A principal therapeutic intent of exposing a tumor to ionizing radiation is to produce irreversible DNA damage in the tumor cells while sparing the around normal tissues involved. The fast kinetics of cell cycling in the tumor cells decreases the desired-effect and requires reduction in overall treatment time to achieve destruction of the malignant cells with minimal adverse effects on the surrounding non-malignant tissue. The access of molecular cell cycle-targeted therapy may represent a supplement to accelerated fractionation regimens in improving the therapeutic index. Complete depletion of Mad2 protein levels induces mitotic failure, multi-nucleation, and apoptosis in tumor cell utilizing RNA interference. CMT2 counteracts the function of Mad2 and is required for the silencing of the spindle checkpoint. In this study, we identified that CMT2 induces tumor cell death and permanent growth arrest