Evidence map›Paper›PMID 33664496›Full record

ArticleNature cell biology2021

Circular RNA-encoded oncogenic E-cadherin variant promotes glioblastoma tumorigenicity through activation of EGFR-STAT3 signalling.

Xinya Gao, Xin Xia, Fanying Li, Maolei Zhang, Huangkai Zhou, Xujia Wu, Jian Zhong, Zheng Zhao, Kun Zhao, Dawei Liu and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers.

0numbers the graph read from it
0cells of the map it votes in
241citing papers in PubMed
32.0field-weighted citation impact, top 1% 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

241 citing papers in PubMed, 419 citations in OpenAlex.

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181 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Xinya Gao *Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Xin Xia *Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Fanying Li *Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Maolei Zhang *Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Huangkai ZhouDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Xujia WuDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Jian ZhongDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Zheng ZhaoBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Kun ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China.
Dawei LiuDepartment of Pathology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Feizhe XiaoDepartment of Scientific Research Section, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Qiang XuGenomiCare Biotechnology (Shanghai), Shanghai, China.
Tao JiangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Bo LiDepartment of Biochemistry and Molecular Biology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.ORCID http://orcid.org/0000-0002-7979-8339
Shi-Yuan ChengThe Ken and Ruth Davee Department of Neurology, Lou and Jean Malnati Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. shiyuan.cheng@northwestern.edu.ORCID http://orcid.org/0000-0003-1737-0588
Nu ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangdong Translational Medicine Innovation Platform, Guangzhou, China. zhangnu2@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-2817-7065
Sun Yat-sen University · CNCapital Medical University · CNGenomiCare (China) · CNNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activated EGFR signalling drives tumorigenicity in 50% of glioblastoma (GBM). However, EGFR-targeting therapy has proven ineffective in treating patients with GBM, indicating that there is redundant EGFR activation. Circular RNAs are covalently closed RNA transcripts that are involved in various physiological and pathological processes. Herein, we report an additional activation mechanism of EGFR signalling in GBM by an undescribed secretory E-cadherin protein variant (C-E-Cad) encoded by a circular E-cadherin (circ-E-Cad) RNA through multiple-round open reading frame translation. C-E-Cad is overexpressed in GBM and promotes glioma stem cell tumorigenicity. C-E-Cad activates EGFR independent of EGF through association with the EGFR CR2 domain using a unique 14-amino-acid carboxy terminus, thereby maintaining glioma stem cell tumorigenicity. Notably, inhibition of C-E-Cad markedly enhances the antitumour activity of therapeutic anti-EGFR strategies in GBM. Our results uncover a critical role of C-E-Cad in stimulating EGFR signalling and provide a promising approach for treating EGFR-driven GBM.

Indexed as

AnimalsAntigens, CDAntineoplastic AgentsBrain NeoplasmsCadherinsCell Line, TumorCell MovementCell ProliferationErbB ReceptorsFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansMiceMice, NudeNeoplasm InvasivenessAntigens, CDAntineoplastic AgentsCadherinsCDH1 protein, humanEGFR protein, humanErbB ReceptorsRNA, CircularSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID33664496
OpenAlexW3135354451

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.