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UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2A-ATF4 axis
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Lei FANG, Huan QI, Peng WANG, Shiqing WANG, Tianjiao LI, Tian XIA, Hai-long PIAO, Chundong GU. UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2A-ATF4 axis[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2A-ATF4 axis",
author="Lei FANG, Huan QI, Peng WANG, Shiqing WANG, Tianjiao LI, Tian XIA, Hai-long PIAO, Chundong GU",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200144"
}
%0 Journal Article
%T UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2A-ATF4 axis
%A Lei FANG
%A Huan QI
%A Peng WANG
%A Shiqing WANG
%A Tianjiao LI
%A Tian XIA
%A Hai-long PIAO
%A Chundong GU
%J Journal of Zhejiang University SCIENCE B
%V -1
%N -1
%P
%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2200144
TY - JOUR
T1 - UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2A-ATF4 axis
A1 - Lei FANG
A1 - Huan QI
A1 - Peng WANG
A1 - Shiqing WANG
A1 - Tianjiao LI
A1 - Tian XIA
A1 - Hai-long PIAO
A1 - Chundong GU
J0 - Journal of Zhejiang University Science B
VL - -1
IS - -1
SP -
EP -
%@ 1673-1581
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2200144
Abstract: UPF1, as the most critical factor in nonsense-mediated mRNA decay(NMD), regulates tumor-associated molecular pathways in many cancers. However, the role of UPF1 in lung adenocarcinoma (LUAD) amino acid metabolism remains largely unknown. In this study, we found that UPF1 was significantly correlated with a portion of amino acid metabolic pathways in LUAD by integrating bioinformatics and metabolomics. We further confirmed that UPF1 knockdown inhibited activating transcription factor 4 (ATF4) and Ser51 phosphorylation of eukaryotic translation initiation factor 2 Alpha (eIF2A), the core proteins in amino acid metabolism reprogramming. In addition, UPF1 promotes cell proliferation by increasing the amino-acid levels of LUAD cells, which depends on the function of ATF4. Clinically, UPF1 mRNA expression is abnormal in LUAD tissues, and higher expression of UPF1 and ATF4 was significantly correlated with poor overall survival (OS) in LUAD patients. Our findings reveal that UPF1 is a potential regulator of tumor-associated amino acid metabolism and may be a therapeutic target for LUAD.
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