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

Young Sun Lee; Jae Kwang Lee; Yeonju Bae; Bok Soon Lee; Eunju Kim; Chang Hoon Cho; Kanghyun Ryoo; Jiyun Yoo; Chul Ho Kim; Gwan Su Yi; Seok Geun Lee; C. Justin Lee; Sang Soo Kang; Eun Mi Hwang; Jae Yong Park

doi:10.1038/srep26413

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

Young Sun Lee, Jae Kwang Lee, Yeonju Bae, Bok Soon Lee, Eunju Kim, Chang Hoon Cho, Kanghyun Ryoo, Jiyun Yoo, Chul Ho Kim, Gwan Su Yi, Seok Geun Lee, C. Justin Lee, Sang Soo Kang, Eun Mi Hwang, Jae Yong Park

School of Biosystem and Biomedical Science

Research output: Contribution to journal › Article › peer-review

42 Citations (Scopus)

Abstract

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 14-3-3γ as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3γ, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3γ. Gene silencing of 14-3-3γ 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.

Original language	English
Article number	26413
Journal	Scientific reports
Volume	6
DOIs	https://doi.org/10.1038/srep26413
Publication status	Published - 2016 May 23

Bibliographical note

Funding Information:
This work was supported by the Bio-Synergy Research Project (NRF-2014M3A9C4066463) of the Ministry of Science, ICT and Future Planning through the National Research Foundation for J.Y.P. and the KIST institutional program (Project No. 2E25170) for E.M.H.

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title = "Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells",

abstract = "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 14-3-3γ as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3γ, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3γ. Gene silencing of 14-3-3γ 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.",

author = "Lee, {Young Sun} and Lee, {Jae Kwang} and Yeonju Bae and Lee, {Bok Soon} and Eunju Kim and Cho, {Chang Hoon} and Kanghyun Ryoo and Jiyun Yoo and Kim, {Chul Ho} and Yi, {Gwan Su} and Lee, {Seok Geun} and Lee, {C. Justin} and Kang, {Sang Soo} and Hwang, {Eun Mi} and Park, {Jae Yong}",

note = "Funding Information: This work was supported by the Bio-Synergy Research Project (NRF-2014M3A9C4066463) of the Ministry of Science, ICT and Future Planning through the National Research Foundation for J.Y.P. and the KIST institutional program (Project No. 2E25170) for E.M.H.",

year = "2016",

month = may,

day = "23",

doi = "10.1038/srep26413",

language = "English",

volume = "6",

journal = "Scientific reports",

issn = "2045-2322",

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T1 - Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

AU - Lee, Young Sun

AU - Lee, Jae Kwang

AU - Bae, Yeonju

AU - Lee, Bok Soon

AU - Kim, Eunju

AU - Cho, Chang Hoon

AU - Ryoo, Kanghyun

AU - Yoo, Jiyun

AU - Kim, Chul Ho

AU - Yi, Gwan Su

AU - Lee, Seok Geun

AU - Lee, C. Justin

AU - Kang, Sang Soo

AU - Hwang, Eun Mi

AU - Park, Jae Yong

N1 - Funding Information: This work was supported by the Bio-Synergy Research Project (NRF-2014M3A9C4066463) of the Ministry of Science, ICT and Future Planning through the National Research Foundation for J.Y.P. and the KIST institutional program (Project No. 2E25170) for E.M.H.

PY - 2016/5/23

Y1 - 2016/5/23

N2 - 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 14-3-3γ as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3γ, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3γ. Gene silencing of 14-3-3γ 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.

AB - 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 14-3-3γ as a binding partner for anterograde trafficking using yeast two-hybrid screening. The surface expression of ANO1 was enhanced by 14-3-3γ, and the Thr9 residue of ANO1 was critical for its interaction with 14-3-3γ. Gene silencing of 14-3-3γ 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.

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

Abstract

Bibliographical note

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UN SDGs

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