Microtubule-targeting agents (MTAs) in anticancer therapy is because they can cause cell death on extended mitotic arrest, the machinery of controlling mitotic arrest is well defined, while the components handling cell death and factors associated in the networks are still not understood very well. Recently, scientists aimed to systematically assess the relative contribution of individual BCL2 family members to cell death initiation on MTA (BI 2536,ABT-737) treatment with single cell resolution. The work shows that BCL2 and BCLX phosphorylation represents a priming event in mitotic cell death that is triggered by NOXA-dependent MCL1 degradation. The MCL1 decay allows in turn BIM-dependent cell death.
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