Evidence map›Paper›PMID 27102302›Full record

ArticleOncotarget2016

Asparaginyl endopeptidase promotes the invasion and metastasis of gastric cancer through modulating epithelial-to-mesenchymal transition and analysis of their phosphorylation signaling pathways.

Yuehong Cui, Yan Wang, Hong Li, Qian Li, Yiyi Yu, Xiaojing Xu, Bei Xu, Tianshu Liu

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Asparaginyl endopeptidase contributes to cetuximab resistance via MEK/ERK signaling in RAS wide-type metastatic colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Molecular biology and immunology of gastric cancer peritoneal metastasis.Translational gastroenterology and hepatology · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Frontiers in physiology · 2018
    Article
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 1 country.

Yuehong CuiMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Yan WangMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Hong LiMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Qian LiMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Yiyi YuMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaojing XuMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Bei XuMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
Tianshu LiuMedical Oncology Department, Zhongshan Hospital, Fudan University, Shanghai, China.
The First Affiliated Hospital, Sun Yat-sen University · CNFudan University · CNSun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asparaginyl endopeptidase (AEP) is a lysosomal protease and overexpressive in gastric cancer. AEP was higher expressive in peritoneal metastatic loci than that in primary gastric cancer. Then we overexpressed AEP or knocked it down with a lentiviral vector in gastric cancer cell lines and detected the cell cycle arrest and the changes of the invasive and metastatic ability in vitro and in vivo. When AEP was knocked-down, the proliferative, invasive and metastatic capacity of gastric cancer cells were inhibited, and the population of sub-G1 cells increased. The expressive level of twist, which is a transcriptional factor, decreased significantly, and the epithelial markers' expression of EMT, E-cadherin increased, but that of the mesenchymal markers, N-cadherin, β-catenin and Vimentin decreased, if AEP was knocked down. These results showed that AEP could promote invasion and metastasis by modulating EMT. We used phosphorylation-specific antibody microarrays to investigate the mechanism that AEP promotes gastric cancer invasion and metastasis, and found that the phosphorylation level of AKT and MAPK signaling pathways were decreased significantly if AEP was knocked-down. Therefore, AKT and MAPK signaling pathways took part in the modulation.

Indexed as

AnimalsAsparaginyl Endopeptidasebeta CateninCadherinsCell Cycle CheckpointsCell Line, TumorCell ProliferationCysteine EndopeptidasesEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, NudeAsparaginyl Endopeptidasebeta CateninCadherinsCTNNB1 protein, humanCysteine EndopeptidasesNuclear ProteinsProto-Oncogene Proteins c-aktTWIST1 protein, humanTwist-Related Protein 1Vimentinasparaginyl endopeptidaseepithelial-to-mesenchymal transitiongastric cancermetastasissignaling pathway

Identifiers

PMID27102302
PMCPMC5085161
OpenAlexW2502182042

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.