Evidence map›Paper›PMID 32413049›Full record

ArticlePloS one2020

CRISPR-mediated ablation of overexpressed EGFR in combination with sunitinib significantly suppresses renal cell carcinoma proliferation.

Bin Liu, Olivia Adaly Diaz Arguello, Deng Chen, Siwei Chen, Ali Saber, Hidde J Haisma

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 46 citations in OpenAlex.

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  14. Altered proTGFα/cleaved TGFα ratios offer new therapeutic strategies in renal carcinoma.Journal of experimental & clinical cancer research : CR · 2021
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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.

Bin LiuDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.ORCID 0000-0002-3168-8456
Olivia Adaly Diaz ArguelloDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.
Deng ChenDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.
Siwei ChenDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.
Ali SaberDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.
Hidde J HaismaDepartment of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, Groningen, University of Groningen, Groningen, The Netherlands.
University of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor tyrosine kinases, such as VEGFR, PDGFR and EGFR, play important roles in renal cancer. In this study, we investigated EGFR knockout as a therapeutic approach in renal cell carcinoma (RCC). We showed that a renal cell carcinoma cell line (RC21) has higher expression of EGFR as compared to other frequently used cell lines such as HEK293, A549, Hela and DLD1. Ablation of EGFR by CRISPR/Cas9 significantly restrained tumor cell growth and activated the MAPK (pERK1/2) pathway. The VEGFR and PDGFR inhibitor, sunitinib, attenuated the expression of MAPK (pERK1/2) and pAKT induced by EGFR loss and further inhibited EGFR-/- cell proliferation. We showed that loss of EGFR eventually leads to resistance to SAHA and cisplatin. Furthermore, EGFR loss induced G2/M phase arrest and resulted in an increased resistance to TNF-related apoptosis-inducing ligand (TRAIL) in renal cell carcinoma. Thus, ablation of overexpressed EGFR by CRISPR/Cas9 alone or in combination with sunitinib may be a new treatment option for renal cell carcinoma.

Indexed as

CRISPR-Cas SystemsA549 CellsAntineoplastic AgentsApoptosisCarcinoma, Renal CellCell Line, TumorCell ProliferationCisplatinCombined Modality TherapyDrug Resistance, NeoplasmErbB ReceptorsGene Knockout TechniquesGenes, erbB-1HEK293 CellsHeLa CellsHumansAntineoplastic AgentsCisplatinEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsSunitinib

Identifiers

PMID32413049
PMCPMC7228069
OpenAlexW3024136821

What OpenQuestion holds

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LicenceCC BY
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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.