Evidence map›Paper›PMID 39358400›Full record

ArticleScientific reports2024

A novel role for WZ3146 in the inhibition of cell proliferation via ERK and AKT pathway in the rare EGFR G719X mutant cells.

Lanxin Li, Chenyang Liu, Rui Wang, Xiaolin Yang, Xiangkai Wei, Chunhong Chu, Guoliang Zhang, Chenxue Liu, Wenrui Cui, Huixia Xu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Lanxin Li *No.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Chenyang Liu *No.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Rui WangNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Xiaolin YangNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Xiangkai WeiNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Chunhong ChuInstitutes of Traditional Chinese Medicine, School of Pharmacy, Henan University, Kaifeng, 475000, Henan, China.
Guoliang ZhangInstitutes of Traditional Chinese Medicine, School of Pharmacy, Henan University, Kaifeng, 475000, Henan, China.
Chenxue LiuNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Wenrui CuiNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Huixia XuNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Ke WangNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China.
Lei AnNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China. anlei@henu.edu.cn.ORCID 0000-0002-9778-2787
Xiaodong LiNo.115, Ximen Avenue, Translational Medicine Center, Huaihe Hospital of Henan University, Henan University, Kaifeng, 475000, China. hhyylxd2013@126.com.

Funding

Henan Medical Education Research Project WJLX2023101Henan Provincial Science and Technology Research Project 242102311023Henan University Teaching Reform Project HDXJJG2022-146
6 · The paper itself

Abstract

Mutations in the epidermal growth factor receptor (EGFR) gene are common driver oncogenes in non-small cell lung cancer (NSCLC). Studies have shown that afatinib is beneficial for NSCLC patients with rare EGFR mutations. However, the effectiveness of tyrosine kinase inhibitors (TKIs) against the G719X (G719A, G719C and G719S) mutation has not been fully established. Herein, using the CRISPR method, the EGFR G719X mutant cell lines were constructed to assess the sensitivity of the rare mutation G719X in NSCLC. WZ3146, a novel mutation-selective EGFR inhibitor, was conducted transcriptome sequencing and in vitro experiments. The results showed that WZ3146 induced cytotoxic effects, inhibited growth vitality and proliferation via ERK and AKT pathway in the EGFR G719X mutant cells. Our findings suggest that WZ3146 may be a promising treatment option for NSCLC patients with the EGFR exon 18 substitution mutation G719X.

Indexed as

Carcinoma, Non-Small-Cell LungCell ProliferationErbB ReceptorsLung NeoplasmsMutationProto-Oncogene Proteins c-aktAntineoplastic AgentsCell Line, TumorHumansMAP Kinase Signaling SystemProtein Kinase InhibitorsAntineoplastic AgentsEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktCytotoxicologyG719XMutantProliferationWZ3146

Identifiers

PMID39358400
PMCPMC11447065

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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.