Evidence map›Paper›PMID 33237585›Full record

ArticleJournal of cellular and molecular medicine2021

G protein-coupled oestrogen receptor promotes cell growth of non-small cell lung cancer cells via YAP1/QKI/circNOTCH1/m6A methylated NOTCH1 signalling.

Yi Shen, Chong Li, Lin Zhou, Jian-An Huang

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

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.4field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  8. Estradiol Promotes Endometriosis ProgressionCurrent pharmaceutical biotechnology · 2026
    Article
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  10. Review
  11. Potential regulatory role of the mActa biochimica et biophysica Sinica · 2025
    Review
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  14. Article
  15. Article
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  18. Circular RNAs Regulate Transcription and Translation.Advances in experimental medicine and biology · 2025
    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

4 authors at 1 institution in 1 country.

Yi ShenDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-4162-5176
Chong LiDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Lin ZhouDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Jian-An HuangDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Results from various studies reveal that the role of G protein-coupled oestrogen receptor (GPER) is cancer-context dependent, and the function of GPER in non-small-cell lung cancer (NSCLC) is still unclear. The present study demonstrated that neoplasm lung tissues expressed higher level of GPER compared with the normal lung tissues. The clinical data also showed that GPER expression level was positively correlated with the tumour stage of NSCLC. Our experimental data confirmed that GPER played an oncogenic role to promote cell growth of NSCLC cells. Mechanistic dissection revealed that GPER could modulate the NOTCH1 pathway to regulate cell growth in NSCLC cells. Further exploration of the mechanism demonstrated that GPER could up-regulate circNOTCH1, which could compete with NOTCH1 mRNA for METTL14 binding. Because of the lack of m6A modification by METTL14 on the NOTCH1 mRNA, NOTCH1 mRNA was more stable and much easier to undergo protein translation. Subsequently, we found that GPER could prevent YAP1 phosphorylation and promote YAP1-TEAD's transcriptional regulation on QKI, a transacting RNA-binding factor involved in circRNA biogenesis, to facilitate circNOTCH1 generation. Supportively, data from preclinical mice model with implantation of H1299 cells also demonstrated that knock-down of circNOTCH1 could block GPER-induced NOTCH1 to suppress NSCLC tumour growth. Together, our data showed that GPER could promote NSCLC cell growth via regulating the YAP1/QKI/circNOTCH1/m6A methylated NOTCH1 pathway, and targeting our identified molecules may be a potentially therapeutic approach to suppress NSCLC development.

Indexed as

A549 CellsAdaptor Proteins, Signal TransducingBlotting, WesternCarcinoma, Non-Small-Cell LungCell ProliferationChromatin ImmunoprecipitationGene Expression Regulation, NeoplasticHumansImmunoprecipitationLung NeoplasmsMethyltransferasesReceptor, Notch1Receptors, EstrogenReceptors, G-Protein-CoupledRNA-Binding ProteinsSignal TransductionAdaptor Proteins, Signal TransducingMethyltransferasesMETTL14 protein, humanNOTCH1 protein, humanQKI protein, humanReceptor, Notch1Receptors, EstrogenReceptors, G-Protein-CoupledRNA-Binding ProteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteinscircular RNAGPERNOTCH1NSCLC

Identifiers

PMID33237585
PMCPMC7810948
OpenAlexW3107040000

What OpenQuestion holds

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LicenceCC BY
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.