Evidence map›Paper›PMID 18832597›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Human rhomboid family-1 gene RHBDF1 participates in GPCR-mediated transactivation of EGFR growth signals in head and neck squamous cancer cells.

Huafei Zou, Sufi M Thomas, Zhen-Wen Yan, Jennifer R Grandis, Andreas Vogt, Lu-Yuan Li

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

47 citing papers in PubMed, 98 citations in OpenAlex.

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  12. Inactive rhomboid proteins RHBDF1 and RHBDF2 (iRhoms): a decade of research in murine models.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
    Review
  13. Article
  14. Review
  15. iRhom2: An Emerging Adaptor Regulating Immunity and Disease.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Review
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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.

Huafei ZouDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Sufi M Thomas
Zhen-Wen Yan
Jennifer R Grandis
Andreas Vogt
Lu-Yuan Li
UPMC Hillman Cancer Center · USUniversity of Pittsburgh · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2004 to 2026
$49.6M
TRADITIONAL AND FLUOROUS SYNTHESIS APPROACHES TO DICTYOSTATIN ANTICANCER AGENTSP01CA078039 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAZO, JOHN S. · 1998 to 2009
$9.9M
GRPR Signaling in SCCHN: Integration with EGFRR01CA098372 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRANDIS, JENNIFER RUBIN · 2004 to 2017
$3.8M
NCI NIH HHS P01 CA078039NCI NIH HHS P01CA78039NCI NIH HHS P50 CA097190NCI NIH HHS P50CA097190NCI NIH HHS R01 CA098372NCI NIH HHS R01CA098372
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) is an activated oncogene in many cancers. It can be transactivated by ligands of G protein-coupled receptors (GPCRs). We show here that a novel gene, human rhomboid family-1 (RHBDF1), which was recently reported to have a pivotal role in epithelial cancer cell growth in culture and in xenograft tumors, participates in the modulation of GPCR-mediated EGFR transactivation. The RHBDF1 protein localizes mainly in the endoplasmic reticulum. Silencing the RHBDF1 gene in head and neck squamous cancer cell line 1483 cells with siRNA causes an inhibition of gastrin-releasing peptide (GRP) -induced phosphorylation of EGFR and EGFR-dependent signaling proteins p44/42 MAPK and AKT, accompanied by an inhibition of GRP-induced survival, proliferation, and invasion of the cells. The EGFR signaling pathway itself remains intact, however, as the cells remain responsive to exogenous EGF. In addition, RHBDF1 gene silencing disrupts GRP-stimulated secretion of EGFR ligand TGF-alpha, but not the production of latent TGF-alpha, whereas engineered overexpression of RHBDF1 markedly accelerates the secretion of TGF-alpha. These findings are consistent with the view that RHBDF1 is critically involved in a GPCR ligand-stimulated process leading to the activation of latent EGFR ligands.

Indexed as

Signal TransductionTranscriptional ActivationCell Line, TumorCell ProliferationEndoplasmic ReticulumErbB ReceptorsGastrin-Releasing PeptideGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansLigandsMembrane ProteinsNeoplasm InvasivenessNeoplasms, Squamous CellReceptors, G-Protein-CoupledRNA, Small InterferingErbB ReceptorsGastrin-Releasing PeptideLigandsMembrane ProteinsReceptors, G-Protein-CoupledRHBDF1 protein, humanRNA, Small InterferingTransforming Growth Factor alpha

Identifiers

PMID18832597
PMCPMC2638965
OpenAlexW2044990701

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.