Abstract
Abstract The pro-death Bcl-2 family protein and tumor suppressor Bax is frequently mutated in tumors with microsatellite instability (MSI). Recently, we identified a novel Bax homolog, BaxΔ2, which is generated by a unique combination of mutation and alternative splicing in MSI tumors. BaxΔ2 is a potent cell death inducer. Unlike the parental Baxα, BaxΔ2 does not directly target to mitochondria, rather activates the caspase 8-mediated mitochondrial pathway. BaxΔ2-positive cancer cells are less invasive and more sensitive to a sub-set of chemotherapeutic agents. Thus, our data provide evidence that gain-of-function BaxΔ2 mutant resulted from mutation and aberrant splicing may be detrimental to tumor and thereby could be beneficial for treatment of cancer. Citation Format: Honghong Zhang, Bonnie Haferkamp, Jialing Xiang. Bax delta2: A gain-of-function Bax mutant for selective chemotherapy. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1711. doi:10.1158/1538-7445.AM2013-1711 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Published Version
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