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A novel regulator of ER Ca2+ drives Hippo-mediated tumorigenesis

Calcium ion (Ca2+) is a versatile second messenger that regulates various cellular and physiological functions. However, the in vivo molecular mechanisms by which Ca2+ alterations contribute to tumor growth remain poorly explored. Here we show that Emei is a novel ER Ca2+ regulator that synergizes w...

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Main Authors: Ma, Xianjue (Author) , Lu, Jin-Yu (Author) , Moraru, Alexandra (Author) , Teleman, Aurelio A. (Author) , Fang, Jinan (Author) , Qiu, Yue (Author) , Liu, Peng (Author) , Xu, Tian (Author)
Format: Article (Journal)
Language:English
Published: 2020
In: Oncogene
Year: 2019, Volume: 39, Issue: 6, Pages: 1378-1387
ISSN:1476-5594
DOI:10.1038/s41388-019-1076-z
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s41388-019-1076-z
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s41388-019-1076-z
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Author Notes:Xianjue Ma, Jin-Yu Lu, Alexandra Moraru, Aurelio A. Teleman, Jinan Fang, Yue Qiu, Peng Liu, Tian Xu
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Summary:Calcium ion (Ca2+) is a versatile second messenger that regulates various cellular and physiological functions. However, the in vivo molecular mechanisms by which Ca2+ alterations contribute to tumor growth remain poorly explored. Here we show that Emei is a novel ER Ca2+ regulator that synergizes with RasV12 to induce tumor growth via JNK-mediated Hippo signaling. Emei disruption reduces ER Ca2+ level and subsequently leads to JNK activation and Hippo inactivation. Importantly, genetically increasing cytosolic Ca2+ concentration cooperates with RasV12 to drive tumor growth via inactivating the Hippo pathway. Finally, we identify POSH as a crucial link that bridges cytosolic Ca2+ alteration with JNK activation and Hippo-mediated tumor growth. Together, our findings provide a novel mechanism of tumor growth that acts through intracellular Ca2+ levels to modulate JNK-mediated Hippo signaling.
Item Description:Published online: 24 October 2019
Im Titel ist "2+" hochgestellt
Gesehen am 24.06.2020
Physical Description:Online Resource
ISSN:1476-5594
DOI:10.1038/s41388-019-1076-z

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