Evidence map›Paper›PMID 27121204›Full record

ArticleOncotarget2016

AURKA induces EMT by regulating histone modification through Wnt/β-catenin and PI3K/Akt signaling pathway in gastric cancer.

Xi Liu, Zhaoxia Li, Yue Song, Rui Wang, Lei Han, Qixue Wang, Kui Jiang, Chunsheng Kang, Qingyu Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 102 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Xi LiuDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Zhaoxia LiDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Yue SongDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Rui WangDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Lei HanLaboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin 300052, China.
Qixue WangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Kui JiangDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Chunsheng KangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Qingyu ZhangDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Tianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer, a highly invasive and aggressive malignancy, is the third leading cause of death from cancer worldwide. Genetic association studies have successfully revealed several important genes consistently associated with gastric cancer to date. However, these robust gastric cancer-associated genes do not fully elucidate the mechanisms underlying the development and progression of the disease. In the present study, we performed an alternative approach, a gene expression-based genome-wide association study (eGWAS) across 13 independent microarray experiments (including 251 gastric cancer cases and 428 controls), to identify top candidates (p<0.00001). Additionally, we conducted gene ontology analysis, pathway analysis and network analysis and identified aurora kinase A (AURKA) as our candidate. We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the β-catenin and the phosphorylation of Akt1 and GSK-3β, as well as blocked the Akt and Wnt signaling pathways. Furthermore, MLN8237 arrested the cells in the G2/M phase. The activity of Wnt and Akt signaling pathways affected the level of histone methylation significantly, and we supposed that MLN8237 affected the level of histone methylation through these two signaling pathways. Additionally, the treatment of MLN8237 influenced the level of H3K4 me1/2/3 and H3K27 me1/2/3. Chip data on cell lines suggested that MLN8237 increases the level of H3K27 me3 on the promoter of Twist and inhibits EMT (epithelial-mesenchymal transition). In summary, AURKA is a potential therapeutic target in gastric cancer and induces EMT through histone methylation.

Indexed as

AnimalsAurora Kinase AAzepinesbeta CateninCaco-2 CellsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHistone CodeHumansMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedPhosphatidylinositol 3-KinasesAurora Kinase AAzepinesbeta CateninMLN 8237Phosphatidylinositol 3-KinasesPyrimidinesAURKAhistone modificationPI3K/Akt pathwayWnt/β-catenin pathway

Identifiers

PMID27121204
PMCPMC5078082
OpenAlexW2342252259

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.