Oncotarget

Reviews:

Exon 3 mutations of CTNNB1 drive tumorigenesis: a review

Chao Gao, Yingmei Wang, Russell Broaddus, Longhao Sun, Fengxia Xue and Wei Zhang _

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Oncotarget. 2018; 9:5492-5508. https://doi.org/10.18632/oncotarget.23695

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Abstract

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

Correspondence to:

Wei Zhang, email: wezhang@wakehealth.edu

Fengxia Xue, email: fengxiaxue1962@163.com

Keywords: β-catenin; CTNNB1; mutations; Wnt/β-catenin signaling pathway; immunosuppression

Received: September 07, 2017    Accepted: November 05, 2017    Published: November 24, 2017

ABSTRACT

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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