Evidence map›Paper›PMID 28991229›Full record

ArticleOncogene2018

Hypoxia activates cadherin-22 synthesis via eIF4E2 to drive cancer cell migration, invasion and adhesion.

N J Kelly, J F A Varga, E J Specker, C M Romeo, B L Coomber, J Uniacke

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  3. The 4EHP-mediated translational repression of cGAS impedes the host immune response against DNA viruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  4. Construction of a Diagnostic mBiomolecules · 2023
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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 1 institution in 1 country.

N J KellyDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada.
J F A VargaDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada.
E J SpeckerDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada.
C M RomeoDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada.
B L CoomberDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada.
J UniackeDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada.
University of Guelph · CA

Funding

CIHR 152925-1
6 · The paper itself

Abstract

Hypoxia is a driver of cell movement in processes such as development and tumor progression. The cellular response to hypoxia involves a transcriptional program mediated by hypoxia-inducible factors, but translational control has emerged as a significant contributor. In this study, we demonstrate that a cell-cell adhesion molecule, cadherin-22, is upregulated in hypoxia via mTORC1-independent translational control by the initiation factor eIF4E2. We identify new functions of cadherin-22 as a hypoxia-specific cell-surface molecule involved in cancer cell migration, invasion and adhesion. Silencing eIF4E2 or cadherin-22 significantly impaired MDA-MB-231 breast carcinoma and U87MG glioblastoma cell migration and invasion only in hypoxia, while reintroduction of the respective exogenous gene restored the normal phenotype. Cadherin-22 was evenly distributed throughout spheroids and required for their formation and support of a hypoxic core. Conversely, E-cadherin translation was repressed by hypoxia and only expressed in the oxygenated cells of U87MG spheroids. Furthermore, immunofluorescence on paraffin-embedded human tissue from 40 glioma and 40 invasive ductal breast carcinoma patient specimens revealed that cadherin-22 expression colocalized with areas of hypoxia and significantly correlated with tumor grade and progression-free survival or stage and tumor size, respectively. This study broadens our understanding of tumor progression and metastasis by highlighting cadherin-22 as a potential new target of cancer therapy to disable hypoxic cancer cell motility and adhesion.

Indexed as

Antigens, CDBreast NeoplasmsCadherinsCarcinoma, Ductal, BreastCell AdhesionCell HypoxiaCell Line, TumorCell MovementDisease ProgressionEukaryotic Initiation Factor-4EFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGliomaHumansMechanistic Target of Rapamycin Complex 1Antigens, CDCadherinsCDH1 protein, humanCDH22 protein, humanEIF4E2 protein, humanEukaryotic Initiation Factor-4EMechanistic Target of Rapamycin Complex 1RNA Cap-Binding ProteinsRNA, MessengerRNA, Small Interfering

Identifiers

PMID28991229
PMCPMC5770212
OpenAlexW2762180380

What OpenQuestion holds

Textmetadata
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.