Suppression of 14-3-3 gamma-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

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Anoctamin-1 (ANO1) acts as a Ca2+-activated Cl- channel in various normal tissues, and its expression is increased in several different types of cancer. Therefore, understanding the regulation of ANO1 surface expression is important for determining its physiological and pathophysiological functions. However, the trafficking mechanism of ANO1 remains elusive. Here, we report that segment a (N-terminal 116 amino acids) of ANO1 is crucial for its surface expression, and we identified 14-3-3 gamma as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3 gamma, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3 gamma. Gene silencing of 14-3-3 gamma and/or ANO1 demonstrated that suppression of ANO1 surface expression inhibited migration and invasion of glioblastoma cells. These findings provide novel therapeutic implications for glioblastomas, which are associated with poor prognosis
Publisher
NATURE PUBLISHING GROUP
Issue Date
2016-05
Language
English
Article Type
Article
Keywords

ACTIVATED CHLORIDE CHANNEL; CA2+-ACTIVATED CL-CHANNEL; ANOCTAMIN 1 TMEM16A; ION CHANNELS; OVEREXPRESSION; ANO1/TMEM16A; CARCINOMA; INVASION; PROTEIN; GENES

Citation

SCIENTIFIC REPORTS, v.6

ISSN
2045-2322
DOI
10.1038/srep26413
URI
http://hdl.handle.net/10203/209491
Appears in Collection
BiS-Journal Papers(저널논문)
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