BCL-XL, and more generally the BCL-2 family members, are not only key regulators of apoptosis, but also actively participate in the regulation of other vital cellular functions.1
In vitro models have shown BCL-XL overexpression increases in vitro cell migration and invasion and facilitates tumor cells to form de novo vasculogenic structures. Furthermore, BCL-XL overexpressing cells exhibit higher tumors sphere formation capacity and express higher levels of stem cell markers, supporting the concept that BCL-XL plays essential roles in the maintenance of cancer stem cell phenotype.1
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