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The Mechanistic Role of the Calcium-Activated Chloride Channel ANO1 in Tumor Growth and Signaling

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Part of the book series: Advances in Experimental Medicine and Biology ((PROTRE,volume 966))

Abstract

Multiple studies have described the high expression and amplification of Anoctamin 1 (ANO1) in various cancers, including, but not limited to breast cancer, head and neck cancer, gastrointestinal stromal tumors and glioblastoma. ANO1 has been demonstrated to be critical for tumor growth in breast and head and neck cancers through its regulation of EGFR signaling and pathway modulators like MAPK and protein kinase B. However, the discovery of ANO1 as a calcium activated chloride channel came as a surprise to the field and has given rise to many questions. How does a chloride channel promote oncogenesis? Is the chloride channel function of ANO1 important for its role in cancer? Does ANO1 exhibits chloride-independent functions in cancer cells? This review summarizes the current understanding of ANO1’s function in cancer, provides a synopsis of the findings addressing the open questions in the field and gives an outlook on the promising future of ANO1 as a potential therapeutic target for the treatment of various cancers.

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Abbreviations

AKT:

protein kinase B

ANO1:

Anoctamin 1

CaCC:

calcium activated chloride channel

CaCC-inh:

calcium activated chloride channel inhibitor

CAMK:

calmodulin dependent kinase

EGFR:

epidermal growth factor receptor

ESCC:

esophageal squamous cell carcinoma

HNSCC:

head and neck squamous cell carcinoma

MAPK:

mitogen-activated kinase

SCC:

squamous cell carcinoma

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All authors are employees of Novartis Institutes for BioMedical Research.

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This article does not contain any studies with human participants or animals performed by any of the authors.

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Correspondence to Larry Alex Gaither .

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Bill, A., Alex Gaither, L. (2017). The Mechanistic Role of the Calcium-Activated Chloride Channel ANO1 in Tumor Growth and Signaling. In: Atassi, M. (eds) Protein Reviews. Advances in Experimental Medicine and Biology(), vol 966. Springer, Singapore. https://doi.org/10.1007/5584_2016_201

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