Evidence map›Paper›PMID 27689325›Full record

ArticleOncotarget2016

Catalytically defective receptor protein tyrosine kinase PTK7 enhances invasive phenotype by inducing MMP-9 through activation of AP-1 and NF-κB in esophageal squamous cell carcinoma cells.

Won-Sik Shin, Yuri Hong, Hae Won Lee, Seung-Taek Lee

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Catalytically inactive receptor tyrosine kinase PTK7 activates FGFR1 independent of FGF.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

4 authors at 2 institutions in 1 country.

Won-Sik ShinDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Yuri HongDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Hae Won LeeDepartment of Thoracic Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Seung-Taek LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Yonsei University · KRKorea Institute of Radiological and Medical Sciences · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein tyrosine kinase 7 (PTK7), a member of the catalytically defective receptor protein tyrosine kinase family, is upregulated in various cancers including esophageal squamous cell carcinoma (ESCC). Here, we have explored the molecular mechanism of PTK7-dependent invasiveness in ESCC cells. PTK7 knockdown reduced gelatin degradation and MMP-9 secretion in cultures of ESCC TE-10 cells, and showed reduced levels of MMP9 mRNA using real-time RT-PCR and luciferase reporter assays. PTK7 knockdown decreased not only phosphorylation of NF-κB, IκB, ERK, and JNK, but also nuclear localization of NF-κB and AP-1 consisting of c-Fos and c-Jun. Activation of AP-1 and NF-κB requires PTK7-mediated activation of tyrosine kinases, including Src. In addition, NF-κB activation by PTK7 involves the PI3K/Akt signaling pathway. PTK7-mediated upregulation of MMP9 was also observed in other ESCC cell lines and in three-dimensional cultures of TE-10 cells. Moreover, MMP-9 expression positively correlated with PTK7 expression in ESCC tumor tissue. These findings demonstrate that PTK7 upregulates MMP9 through activation of AP-1 and NF-κB and, thus increases invasive properties of ESCC cells.

Indexed as

Carcinoma, Squamous CellCell Adhesion MoleculesCell Line, TumorEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Knockdown TechniquesHumansImmunohistochemistryMatrix Metalloproteinase 9Neoplasm InvasivenessNF-kappa BPhenotypePhosphatidylinositol 3-KinasesPhosphorylationProteolysisProto-Oncogene Proteins c-aktCell Adhesion MoleculesMatrix Metalloproteinase 9NF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTK7 protein, humanReceptor Protein-Tyrosine KinasesRNA, Messengersrc-Family KinasesTranscription Factor AP-1AP-1esophageal squamous cell carcinoma (ESCC)MMP-9NF-κBPTK7

Identifiers

PMID27689325
PMCPMC5341976
OpenAlexW2523810079

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.