Evidence map›Paper›PMID 32827244›Full record

ArticleJournal of cellular and molecular medicine2020

Up-regulated acylglycerol kinase (AGK) expression associates with gastric cancer progression through the formation of a novel YAP1-AGK-positive loop.

Shanshan Huang, Yuan Cao, Hui Guo, Yangyang Yao, Li Li, Jun Chen, Junhe Li, Xiaojun Xiang, Jun Deng, Jianping Xiong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

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  13. Acylglycerol Kinase-Targeted Therapies in Oncology.Frontiers in cell and developmental biology · 2021
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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

10 authors at 1 institution in 1 country.

Shanshan HuangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Yuan CaoDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Hui GuoDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Yangyang YaoDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Li LiDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Jun ChenDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Junhe LiDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Xiaojun XiangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Jun DengDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0002-7644-5853
Jianping XiongDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0003-0398-6090
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acylglycerol kinase (AGK) uses adenosine triphosphate (ATP) and acylglycerol to generate adenosine diphosphate (ADP) and acyl-sn-glycerol 3-phosphate in cells. Recent evidence has demonstrated that dysregulated AGK expression is associated with the development of various human cancers. This study investigated the effects of AGK on gastric cancer cell proliferation and carcinogenesis and explored the underlying molecular events. AGK expression was up-regulated in gastric cancer and was associated with poor prognosis in gastric cancer patients. AGK overexpression increased gastric cancer proliferation, invasion capacity and the expression of the epithelial-mesenchymal transition markers in vitro. Conversely, the knockdown of AGK expression reduced gastric cancer cell proliferation in vitro and in nude mouse tumour cell xenografts. Importantly, AGK expression was associated with the YAP1 expression in gastric cancer cells and tissues. YAP1 expression also transcriptionally induced AGK expression through the binding of TEAD to the AGK gene promoter. However, AGK expression inhibited the activation of the Hippo pathway proteins and induced YAP1 nuclear localization to enhance the transcription activity of YAP1/TEADs. In conclusion, the study demonstrates that AGK is not only a novel target of the Hippo-YAP1 pathway, but that it also positively regulates YAP1 expression, thus forming a YAP1-AGK-positive feedback loop.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, EnzymologicHEK293 CellsHumansMice, NudeNeoplasm InvasivenessPhosphotransferases (Alcohol Group Acceptor)Stomach NeoplasmsTranscription FactorsTranscription, Geneticacylglycerol kinaseAdaptor Proteins, Signal TransducingPhosphotransferases (Alcohol Group Acceptor)Transcription FactorsYAP1 protein, humanYAP-Signaling ProteinsAGKbiomarkergastric cancerHippo-YAP1 pathway

Identifiers

PMID32827244
PMCPMC7576242
OpenAlexW3081476640

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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.