Exon 3 mutations of CTNNB1 drive tumorigenesis: a review
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Chao Gao1,2,3,*, Yingmei Wang1,*, Russell Broaddus2, Longhao Sun3, Fengxia Xue1 and Wei Zhang2,3
1Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China
2Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
3Department of Cancer Biology, Wake Forest Baptist Comprehensive Cancer Center, Winston-Salem, NC, USA
*These authors have contributed equally to this work
Wei Zhang, email: [email protected]
Fengxia Xue, email: [email protected]
Keywords: β-catenin; CTNNB1; mutations; Wnt/β-catenin signaling pathway; immunosuppression
Received: September 07, 2017 Accepted: November 05, 2017 Published: November 24, 2017
The canonical Wnt/β-catenin signaling pathway, an important modulator of progenitor cell proliferation and differentiation, is highly regulated for the maintenance of critical biological homeostasis. Decades of studies in cancer genetics and genomics have demonstrated that multiple genes encoding key proteins in this signaling pathway serve as targets for recurrent mutational alterations. Among these proteins, β-catenin and adenomatosis polyposis coli (APC) are two key nodes. β-catenin contributes in transporting extracellular signals for nuclear programming. Mutations of the CTNNB1 gene that encodes β-catenin occur in a wide spectrum of cancers. These mutations alter the spatial characteristics of the β-catenin protein, leading to drastic reprogramming of the nuclear transcriptional network. Among the outcomes of this reprogramming are increased cell proliferation, enhanced immunosuppression, and disruption of metabolic regulation. Herein we review the current understanding of CTNNB1 mutations, their roles in tumorigenesis and discuss their possible therapeutic implications for cancer.
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