Evidence map›Paper›PMID 37341071›Full record

ArticleCancer medicine2023

Inhibition of VEGFR2 and EGFR signaling cooperatively suppresses the proliferation of oral squamous cell carcinoma.

Maho Onda, Akinobu Ota, Kunihiro Ito, Takayuki Ono, Sivasundaram Karnan, Mikako Kato, Sayuri Kondo, Akifumi Furuhashi, Tomio Hayashi, Yoshitaka Hosokawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 13 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

11 authors at 3 institutions in 1 country.

Maho OndaDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Akinobu OtaDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.ORCID 0000-0002-6296-2921
Kunihiro ItoDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Takayuki OnoDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Sivasundaram KarnanDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.ORCID 0000-0003-2165-7565
Mikako KatoDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Sayuri KondoDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Akifumi FuruhashiDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Tomio HayashiDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Yoshitaka HosokawaDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Yoshiaki KazaokaDepartment of Oral and Maxillofacial Surgery, Aichi Medical University Hospital, Nagakute, Japan.
Aichi Medical University Hospital · JPAichi Medical University · JPKinjo Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpidermal growth factor receptor (EGFR) is frequently overexpressed in oral squamous cell carcinoma (OSCC), and EGFR-targeting therapeutics have been widely employed to treat patients with a variety of carcinomas including OSCC. Here, we aimed to investigate alternative signaling for OSCC survival under the disruption of EGFR signaling.

methodsOSCC cell lines, namely HSC-3 and SAS, were utilized to investigate how EGFR disruption affects cell proliferation. Gene set enrichment analysis was performed to examine how EGFR disruption affects oncogenic signaling in OSCC cells. Disruption of KDR gene was performed using CRISPR/Cas9 techniques. A VEGFR inhibitor, vatalanib was used to research the impact of VEGFR inhibition on OSCC survival.

resultsEGFR disruption significantly decreased the proliferation and oncogenic signaling including Myc and PI3K-Akt, in OSCC cells. Chemical library screening assays revealed that VEGFR inhibitors continued to inhibit the proliferation of EGFR-deficient OSCC cells. In addition, CRISPR-mediated disruption of KDR/VEGFR2 retarded OSCC cell proliferation. Furthermore, combined erlotinib-vatalanib treatment exhibited a more potent anti-proliferative effect on OSCC cells, compared to either monotherapy. The combined therapy effectively suppressed the phosphorylation levels of Akt but not p44/42.

conclusionVEGFR-mediated signaling would be an alternative signaling pathway for the survival of OSCC cells under the disruption of EGFR signaling. These results highlight the clinical application of VEGFR inhibitors in the development of multi-molecular-targeted therapeutics against OSCC.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMouth NeoplasmsCell Line, TumorCell ProliferationErbB ReceptorsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSquamous Cell Carcinoma of Head and NeckEGFR protein, humanErbB ReceptorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktdrug sensitivityEGFRgenome editingOSCCVEGFR

Identifiers

PMID37341071
PMCPMC10469792
OpenAlexW4381469454

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.