Evidence map›Paper›PMID 25514462›Full record

ArticleOncotarget2015

Claudin-7 promotes the epithelial-mesenchymal transition in human colorectal cancer.

Rahel Philip, Sarah Heiler, Wei Mu, Markus W Büchler, Margot Zöller, Florian Thuma

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 76 citations in OpenAlex.

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  14. Claudins as biomarkers of differential diagnosis and prognosis of tumors.Journal of cancer research and clinical oncology · 2021
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  19. Targeting claudins in cancer: diagnosis, prognosis and therapy.American journal of cancer research · 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

6 authors at 2 institutions in 1 country.

Rahel PhilipDepartment of Tumor Cell Biology, University Hospital of Surgery, Heidelberg.
Sarah HeilerDepartment of Tumor Cell Biology, University Hospital of Surgery, Heidelberg.
Wei MuDepartment of Tumor Cell Biology, University Hospital of Surgery, Heidelberg.
Markus W BüchlerUniversity Hospital of General Surgery, Heidelberg.
Margot ZöllerDepartment of Tumor Cell Biology, University Hospital of Surgery, Heidelberg.
Florian ThumaDepartment of Tumor Cell Biology, University Hospital of Surgery, Heidelberg.
University Hospital Heidelberg · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In colorectal cancer (CoCa) EpCAM is frequently associated with claudin-7. There is evidence that tumor-promoting EpCAM activities are modulated by the association with claudin-7. To support this hypothesis, claudin-7 was knocked-down (kd) in HT29 and SW948 cells. HT29-cld7kd and SW948-cld7kd cells display decreased anchorage-independent growth and the capacity for holoclone-, respectively, sphere-formation is reduced. Tumor growth is delayed and cld7kd cells poorly metastasize. In line with this, migratory and invasive potential of cld7kd clones is strongly impaired, migration being inhibited by anti-CD49c, but not anti-EpCAM, although motility is reduced in EpCAM siRNA-treated cells. This is due to claudin-7 recruiting EpCAM in glycolipid-enriched membrane fractions towards claudin-7-associated TACE and presenilin2, which cleave EpCAM. The cleaved intracellular domain, EpIC, promotes epithelial-mesenchymal transition (EMT)-associated transcription factor expression, which together with fibronectin and vimentin are reduced in claudin-7kd cells. But, uptake of HT29wt and SW948wt exosomes by the claudin-7kd lines sufficed for transcription factor upregulation and for restoring motility. Thus, claudin-7 contributes to motility and invasion and is required for recruiting EpCAM towards TACE/presenilin2. EpIC generation further supports motility by promoting a shift towards EMT. Notably, EMT features of cld7-competent metastatic CoCa cells can be transferred via exosomes to poorly metastatic cells.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionAnimalsAntigens, NeoplasmBlotting, WesternCell AdhesionCell Adhesion MoleculesCell Line, TumorCell ProliferationClaudinsColorectal NeoplasmsEpithelial Cell Adhesion MoleculeExosomesHT29 CellsHumansMice, SCIDAntigens, NeoplasmCell Adhesion MoleculesClaudinsCLDN7 protein, humanEpithelial Cell Adhesion Molecule

Identifiers

PMID25514462
PMCPMC4385835
OpenAlexW1525870544

What OpenQuestion holds

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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.