Evidence map›Paper›PMID 34791835›Full record

ArticleCancer reports (Hoboken, N.J.)2022

The effects of CD148 Q276P/R326Q polymorphisms in A431D epidermoid cancer cell proliferation and epidermal growth factor receptor signaling.

Lilly He, Keiko Takahashi, Lejla Pasic, Chikage Narui, Philipp Ellinger, Manuel Grundmann, Takamune Takahashi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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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

7 authors at 3 institutions in 2 countries.

Lilly HeDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Keiko TakahashiDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Lejla PasicDepartment of Biochemistry, Vanderbilt University, Nashville, Tennessee, USA.
Chikage NaruiDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Philipp EllingerBayer AG Research & Development, Pharmaceuticals, Wuppertal, Germany.
Manuel GrundmannBayer AG Research & Development, Pharmaceuticals, Wuppertal, Germany.
Takamune TakahashiDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID 0000-0002-4841-2499
Vanderbilt University Medical Center · USBayer (Germany) · DEVanderbilt University · US

Funding

Role of CD148 Tyrosine Phosphatase in Diabetic NephropathyR01DK097332 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI TAKAHASHI, TAKAMUNE · 2012 to 2016
$1.7M
NIDDK NIH HHS R01 DK097332
6 · The paper itself

Abstract

backgroundCD148 is a transmembrane protein tyrosine phosphatase that is expressed in multiple cell types. Previous studies have shown that CD148 dephosphorylates growth factor receptors and their signaling molecules, including EGFR and ERK1/2, and negatively regulates cancer cell growth. Furthermore, research of clinical patients has shown that highly linked CD148 gene polymorphisms, Gln276Pro (Q276P) and Arg326Gln (R326Q), are associated with an increased risk of several types of cancer. However, the biological effects of these missense mutations have not been studied.

aimWe aimed to determine the biological effects of CD148 Q276P/R326Q mutations in cancer cell proliferation and growth factor signaling, with emphasis on EGFR signaling.

methodsCD148 forms, wild-type (WT) or Q276P/R326Q, were retrovirally introduced into A431D epidermoid carcinoma cells that lacks CD148 expression. The stable cells that express comparable levels of CD148 were sorted by flow cytometry. A431D cells infected with empty retrovirus was used as a control. CD148 localization, cell proliferation rate, EGFR signaling, and the response to thrombospondin-1 (TSP1), a CD148 ligand, were assessed by immunostaining, cell proliferation assay, enzyme-linked immunosorbent assay, and Western blotting.

resultsBoth CD148 forms (WT, Q276P/R326Q) were distributed to cell surface and all three cell lines expressed same level of EGFR. Compared to control cells, the A431D cells that express CD148 forms showed significantly lower cell proliferation rates. EGF-induced EGFR and ERK1/2 phosphorylation as well as cell proliferation were also significantly reduced in these cells. Furthermore, TSP1 inhibited cell proliferation in CD148 (WT, Q276P/R326Q)-expressing A431D cells, while it showed no effects in control cells. However, significant differences were not observed between CD148 WT and Q276P/R326Q cells.

conclusionOur data demonstrates that Q276P/R326Q mutations do not have major effects on TSP1-CD148 interaction as well as on CD148's cellular localization and activity to inhibit EGFR signaling and cell proliferation.

Indexed as

Carcinoma, Squamous CellReceptor-Like Protein Tyrosine Phosphatases, Class 3Cell ProliferationErbB ReceptorsHumansPolymorphism, GeneticErbB ReceptorsPTPRJ protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 3A431D cellsCD148cell proliferationEGFRepidermoid cancerpolymorphism

Identifiers

PMID34791835
PMCPMC9458507
OpenAlexW3213762648

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.