Evidence map›Paper›PMID 30732676›Full record

ArticleOncology research2019

NOTCH3 Overexpression and Posttranscriptional Regulation by miR-150 Were Associated With EGFR-TKI Resistance in Lung Adenocarcinoma.

Youwei Zhang, Bi Chen, Yongsheng Wang, Qi Zhao, Weijun Wu, Peiying Zhang, Liyun Miao, Sanyuan Sun

Open access · hybridAbstract read
In one paragraph

Article in Oncology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Construction and clinical significance of prognostic risk markers based on cancer driver genes in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  4. Review
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  7. Review
  8. Article
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  10. Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022
    Review
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  13. 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

8 authors at 3 institutions in 1 country.

Youwei ZhangDepartment of Medical Oncology, Xuzhou Central Hospital, Xuzhou Medical University, Xuzhou, P.R. China.
Bi ChenDepartment of Respiratory Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, P.R. China.
Yongsheng WangDepartment of Respiratory Medicine, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, P.R. China.
Qi ZhaoDepartment of Respiratory Medicine, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, P.R. China.
Weijun WuDepartment of Clinical Pharmacy, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, P.R. China.
Peiying ZhangDepartment of Medical Oncology, Xuzhou Central Hospital, Xuzhou Medical University, Xuzhou, P.R. China.
Liyun MiaoDepartment of Respiratory Medicine, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, P.R. China.
Sanyuan SunDepartment of Medical Oncology, Xuzhou Central Hospital, Xuzhou Medical University, Xuzhou, P.R. China.
Nanjing Drum Tower Hospital · CNXuzhou Central Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are not yet clear. In our study, we found that among four members of NOTCH1-4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then miR-150 was identified as a posttranscriptional regulator of NOTCH3. Its expression was downregulated in LUAD tissues and negatively correlated with NOTCH3 mRNA. The cell proliferation and IC

Indexed as

Protein Processing, Post-TranslationalAdenocarcinoma of LungCell Line, TumorCell ProliferationCollagen Type ICollagen Type I, alpha 1 ChainDrug Resistance, NeoplasmErbB ReceptorsGene Knockdown TechniquesHumansLung NeoplasmsMicroRNAsPrognosisProtein Kinase InhibitorsReceptor, Notch3RNA, MessengerCollagen Type ICollagen Type I, alpha 1 ChainEGFR protein, humanErbB ReceptorsMicroRNAsMIR150, humanNOTCH3 protein, humanProtein Kinase InhibitorsReceptor, Notch3RNA, Messenger

Identifiers

PMID30732676
PMCPMC7848279
OpenAlexW2911274872

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.