Evidence map›Paper›PMID 31076568›Full record

ArticleOncogenesis2019

Phosphorylation of 14-3-3ζ links YAP transcriptional activation to hypoxic glycolysis for tumorigenesis.

Yu Jia, Hui-Yan Li, Jue Wang, Ying Wang, Peng Zhang, Ning Ma, Shi-Jing Mo

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 38 citations in OpenAlex.

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  16. Glycolysis in the progression of pancreatic cancer.American journal of cancer research · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Yu JiaCancer Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430030, Wuhan, Hubei, People's Republic of China.
Hui-Yan LiGeneral Surgical Laboratory, The First Affiliated Hospital, Sun Yat-Sen University, 510080, Guangzhou, Guangdong, People's Republic of China.
Jue WangDepartment of Pathology, The First Affiliated Hospital, Sun Yet-Sen University, 510080, Guangzhou, Guangdong, People's Republic of China.
Ying WangDepartment of Surgery, Huashan Hospital, Fudan University, 200040, Shanghai, People's Republic of China.
Peng ZhangDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, Guangdong, People's Republic of China.
Ning MaGeneral Surgical Laboratory, The First Affiliated Hospital, Sun Yat-Sen University, 510080, Guangzhou, Guangdong, People's Republic of China.
Shi-Jing MoGeneral Surgical Laboratory, The First Affiliated Hospital, Sun Yat-Sen University, 510080, Guangzhou, Guangdong, People's Republic of China. moshij@mail2.sysu.edu.cn.
Sun Yat-sen University · CNHuashan Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CNTongji Hospital · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic microenvironment deregulates metabolic homeostasis in cancer cells albeit the underlying mechanisms involved in this process remain hitherto enigmatic. 14-3-3ζ/Yes-associated protein (YAP) axis plays a principal role in malignant transformation and tumor development. Here, we report that hypoxia disassembles 14-3-3ζ from YAP and thereby promotes YAP nuclear localization mediated by ERK2, which directly binds to the D-site of mitogen-activated protein kinase (MAPK) docking domain in 14-3-3ζ Leu98/100 and phosphorylates 14-3-3ζ at Ser37. When localizing in nucleus, YAP recruits at pyruvate kinase M2 (PKM2) gene promoter with hypoxia-inducible factor 1α (HIF-1α), for which PKM2 transcription is required. 14-3-3ζ Ser37 phosphorylation is instrumental for the hypoxia-induced glucose uptake, lactate production, and clonogenicity of pancreatic ductal adenocarcinoma (PDAC) cells, as well as tumorigenesis in mice. The 14-3-3ζ Ser37 phosphorylation positively correlates with p-ERK1/2 activity and HIF-1α expression in clinical samples from patients with PDAC and predicts unfavorable prognosis. Our findings underscore an appreciable linkage between YAP transcriptional activation and hypoxic glycolysis governed by ERK2-dependent 14-3-3ζ Ser37 phosphorylation for malignant progression of PDAC.

Identifiers

PMID31076568
PMCPMC6510816
OpenAlexW2944077036

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.