NS5ATP9 Promotes Beclin 1‐Dependent Starvation‐Induced Autophagy of Hepatoblastoma Cells
Identifieur interne : 000F38 ( Main/Exploration ); précédent : 000F37; suivant : 000F39NS5ATP9 Promotes Beclin 1‐Dependent Starvation‐Induced Autophagy of Hepatoblastoma Cells
Auteurs : Min Quan [République populaire de Chine] ; Shunai Liu [République populaire de Chine] ; Qi Wang [République populaire de Chine] ; Guoli Li [République populaire de Chine] ; Yu Zhang [République populaire de Chine] ; Shenghu Feng [République populaire de Chine] ; Jinqiu Liang [République populaire de Chine] ; Jun Cheng [République populaire de Chine]Source :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 2015-08.
Abstract
NS5ATP9, a gene up‐regulated by NS5A, plays a crucial oncogenic role in several types of human tumours. However, the underlying mechanisms remain unclear. Autophagy, an evolutionarily conserved catabolic process, maintains cellular homeostasis under stress conditions, such as starvation, and plays a crucial role in tumour initiation and progression. Here, we report that NS5ATP9 mRNA and protein expression was up‐regulated in starved HepG2 cells and that the up‐regulated NS5ATP9 played a functional role in starvation‐induced autophagy. Overexpression or silencing of this gene showed contrasting effects on Beclin 1 and on starvation‐induced autophagy. Furthermore, NS5ATP9‐mediated autophagy is required for promotion of tumour cell growth, and this effect could be inhibited with 3‐methyladenine, chloroquine or by Beclin 1‐silencing. Thus, the mechanism for NS5ATP9‐promoted autophagy is Beclin 1‐dependent in the condition of starvation, and for hepatoblastoma cell growth is also Beclin 1‐dependent. J. Cell. Biochem. 116: 1574–1582, 2015. © 2015 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jcb.25111
Affiliations:
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oncogenic role in several types of human tumours. However, the underlying mechanisms remain unclear. Autophagy, an evolutionarily conserved catabolic process, maintains cellular homeostasis under stress conditions, such as starvation, and plays a crucial role in tumour initiation and progression. Here, we report that NS5ATP9 mRNA and protein expression was up‐regulated in starved HepG2 cells and that the up‐regulated NS5ATP9 played a functional role in starvation‐induced autophagy. Overexpression or silencing of this gene showed contrasting effects on Beclin 1 and on starvation‐induced autophagy. Furthermore, NS5ATP9‐mediated autophagy is required for promotion of tumour cell growth, and this effect could be inhibited with 3‐methyladenine, chloroquine or by Beclin 1‐silencing. Thus, the mechanism for NS5ATP9‐promoted autophagy is Beclin 1‐dependent in the condition of starvation, and for hepatoblastoma cell growth is also Beclin 1‐dependent. J. Cell. Biochem. 116: 1574–1582, 2015. © 2015 Wiley Periodicals, Inc.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Guangdong</li></region><settlement><li>Jiangmen</li><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Quan, Min" sort="Quan, Min" uniqKey="Quan M" first="Min" last="Quan">Min Quan</name></noRegion><name sortKey="Cheng, Jun" sort="Cheng, Jun" uniqKey="Cheng J" first="Jun" last="Cheng">Jun Cheng</name><name sortKey="Cheng, Jun" sort="Cheng, Jun" uniqKey="Cheng J" first="Jun" last="Cheng">Jun Cheng</name><name sortKey="Feng, Shenghu" sort="Feng, Shenghu" uniqKey="Feng S" first="Shenghu" last="Feng">Shenghu Feng</name><name sortKey="Feng, Shenghu" sort="Feng, Shenghu" uniqKey="Feng S" first="Shenghu" last="Feng">Shenghu Feng</name><name sortKey="Li, Guoli" sort="Li, Guoli" uniqKey="Li G" first="Guoli" last="Li">Guoli Li</name><name sortKey="Li, Guoli" sort="Li, Guoli" uniqKey="Li G" first="Guoli" last="Li">Guoli Li</name><name sortKey="Liang, Jinqiu" sort="Liang, Jinqiu" uniqKey="Liang J" first="Jinqiu" last="Liang">Jinqiu Liang</name><name sortKey="Liang, Jinqiu" sort="Liang, Jinqiu" uniqKey="Liang J" first="Jinqiu" last="Liang">Jinqiu Liang</name><name sortKey="Liu, Shunai" sort="Liu, Shunai" uniqKey="Liu S" first="Shunai" last="Liu">Shunai Liu</name><name sortKey="Liu, Shunai" sort="Liu, Shunai" uniqKey="Liu S" first="Shunai" last="Liu">Shunai Liu</name><name sortKey="Quan, Min" sort="Quan, Min" uniqKey="Quan M" first="Min" last="Quan">Min Quan</name><name sortKey="Quan, Min" sort="Quan, Min" uniqKey="Quan M" first="Min" last="Quan">Min Quan</name><name sortKey="Wang, Qi" sort="Wang, Qi" uniqKey="Wang Q" first="Qi" last="Wang">Qi Wang</name><name sortKey="Wang, Qi" sort="Wang, Qi" uniqKey="Wang Q" first="Qi" last="Wang">Qi Wang</name><name sortKey="Zhang, Yu" sort="Zhang, Yu" uniqKey="Zhang Y" first="Yu" last="Zhang">Yu Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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