ArticleJournal of Zhejiang University. Science. B2022
UPF1 increases amino acid levels and promotes cell proliferation in lung adenocarcinoma via the eIF2α-ATF4 axis.
Article in Journal of Zhejiang University. Science. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Gypenosides Mitigate STEC-Induced Intestinal Injury Through Modulation of Ferroptosis Involving the ATF4-CHAC1-GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Nonsense-mediated mRNA decay: a key regulatory system engaged in cancer.Cell communication and signaling : CCS · 2025Review
- Spatial expression of the nonsense-mediated mRNA decay factors UPF3A and UPF3B among mouse tissues.Journal of Zhejiang University. Science. B · 2023Article
- Disulfiram enhances the antitumor activity of cisplatin by inhibiting the Fanconi anemia repair pathway.Journal of Zhejiang University. Science. B · 2023Article
- Cancer immunotherapy: an evolving paradigm.Journal of Zhejiang University. Science. B · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Up-frameshift 1 (UPF1), as the most critical factor in nonsense-mediated messenger RNA (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 2α (eIF2α), 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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