Journal
CELL CYCLE
Volume 12, Issue 24, Pages 3824-3832Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cc.26811
Keywords
spindle assembly checkpoint; Mad2; p31(Comet); Rb; E2F; cell cycle; cancer
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Funding
- Lerner Research Institute
- Ohio Cancer Research Associates
- US National Institutes of Health [R01CA138421]
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p31(Comet) is a well-known interacting partner of the spindle assembly checkpoint (SAC) effector molecule Mad2. At the molecular level it is well established that p31(Comet) promotes efficient mitotic exit, specifically the metaphase-anaphase transition, by antagonizing Mad2 function. However, there is little knowledge of how p31(Comet) is regulated or the physiological importance of controlling p31(Comet). Here, we show that the Rb-E2F pathway regulates p31(Comet) expression. In multiple tumor types (including breast and lung) p31(Comet) expression is increased along with Mad2. expression of this antagonist-target pair is coordinated in cells and correlated in cancer. Moreover, a narrow range of p31(Comet):Mad2 ratios is compatible with cellular viability. our data suggest that coordinate regulation is important for the outgrowth of oncogenic cell populations. our findings suggest that altered p31(Comet):Mad2 expression ratios may provide new insight into altered SAC function and the generation of chromosomal instability in tumors.
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