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Chemosensitivity of Cancer Cells Linked to Protein Dependency
Cancer cells often become dependent on one or more anti-apoptotic proteins to avoid death while continuing to proliferate. BCL-2, for example, is overexpressed in many cancers and mops up pro-apoptotic proteins to prevent them from permeabilizing mitochondria and initiating cell death. Other tumors are reliant on a related protein called MCL-1, but less is known about this member of the BCL-2 family. Brunelle et al. created leukemic mice overexpressing MCL-1 and compared them to similar mice that produced excess BCL-2.
The leukemias suffered by these two types of mice were identical, yet a technique called BH3 profiling was able to distinguish between cells derived from the different animals by demonstrating a dependency on one or other of the two anti-apoptotic proteins. Immunoprecipitation experiments revealed that MCL-1 and BCL-2 both work by sequestering the same two pro-apoptotic targets. Surprisingly then, leukemia cells reliant on MCL-1 were much more sensitive to a range of chemotherapeutic drugs than their BCL-2–dependent counterparts were. Brunelle et al. found that the different cytotoxic drugs all caused a rapid decrease in MCL-1 protein levels via proteosome-mediated degradation, allowing cell death to proceed quickly. BCL-2 protein is more stable however, so additional time and more drug is needed to kill BCL-2–dependent cancer cells.
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