Evidence map›Paper›PMID 29884309›Full record

ArticleCytokine2018

Ablation of the CD9 receptor in human lung cancer cells using CRISPR/Cas alters migration to chemoattractants including IL-16.

David J Blake, Jonathon D Martiszus, Tia H Lone, Steven D Fenster

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. CD9, a tetraspanin target for cancer therapy?Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Effects of Cocaine on Human Glial-Derived Extracellular Vesicles.Frontiers in cell and developmental biology · 2020
    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

4 authors at 1 institution in 1 country.

David J BlakeDepartment of Biology, Fort Lewis College, 1000 Rim Dr, Durango, CO 81301, United States. Electronic address: blake_d@fortlewis.edu.
Jonathon D MartiszusDepartment of Biology, Fort Lewis College, 1000 Rim Dr, Durango, CO 81301, United States.
Tia H LoneDepartment of Biology, Fort Lewis College, 1000 Rim Dr, Durango, CO 81301, United States.
Steven D FensterDepartment of Biology, Fort Lewis College, 1000 Rim Dr, Durango, CO 81301, United States.
Fort Lewis College · US

Funding

Minority Research Training in Biomedical and Behavioral STEM Disciplines at FLCT34GM092711 · NIGMS · FORT LEWIS COLLEGE · PI FENSTER, STEVEN DANIEL · 2010 to 2020
$2.0M
NIGMS NIH HHS T34 GM092711
6 · The paper itself

Abstract

CD9, a member of the tetraspanin superfamily, has been implicated in regulating various physiological processes, including cell motility, adhesion, apoptosis and metastasis. Recently, interleukin-16 (IL-16), a pro-inflammatory cytokine released by normal airway and alveolar epithelial cells, has been implicated as a possible ligand for CD9 as an alternative receptor. In this study, using A549 cells as a model of human alveolar epithelium, CD9 expression was ablated using CRISPR/Cas technology. Decreased expression of CD9 mRNA and protein levels was confirmed through RT-qPCR and flow cytometry, respectively. Individual clones were generated that expressed high levels of CD9 (wild-type, WT) or significantly less CD9 (knockdown, KD). Both wild-type and knockdown A549 cell migration was quantified using a FluoroBloc transwell chemotaxis assay. Our results indicate that wild-type A549 cells migrated towards chemoattractants. Moreover, CD9 expression was required in this process since the CD9 knockdown cells had a significantly reduced migration towards growth serum and IL-16. These results support the migratory properties for CD9 in human lung cells and support the hypothesis that CD9 serves as an alternative receptor for IL-16.

Indexed as

A549 CellsApoptosisCell Line, TumorCell MovementChemotactic FactorsClustered Regularly Interspaced Short Palindromic RepeatsHumansInterleukin-16Lung NeoplasmsMembrane GlycoproteinsSignal TransductionTetraspanin 29CD9 protein, humanChemotactic FactorsInterleukin-16Membrane GlycoproteinsTetraspanin 29A549 cellsCancerCD9CRISPR/Cas technologyInterleukin-16Migration

Identifiers

PMID29884309
PMCPMC8711597
OpenAlexW2807687201

What OpenQuestion holds

Textmetadata
LicenceTDM
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.