Evidence map›Paper›PMID 37542131›Full record

ArticleCancer gene therapy2023

LAMC2 promotes EGFR cell membrane localization and acts as a novel biomarker for tyrosine kinase inhibitors (TKIs) sensitivity in lung cancer.

Dongdong Tong, Xiaofei Wang, Liying Liu, Ting Wen, QiaoYi Chen, Chen Huang

Open access · hybridAbstract read
In one paragraph

Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. LAMC2Cancer science · 2026
    Article
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  5. 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

6 authors at 1 institution in 1 country.

Dongdong TongDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.
Xiaofei WangBiomedical Experimental Center of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China.
Liying LiuBiomedical Experimental Center of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China.
Ting WenDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.
QiaoYi ChenDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China. qychen203@xjtu.edu.cn.ORCID 0000-0003-2911-7424
Chen HuangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China. hchen@xjtu.edu.cn.ORCID 0000-0002-2407-9716
Xi'an Jiaotong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32271006National Natural Science Foundation of China (National Science Foundation of China) 81702918National Natural Science Foundation of China (National Science Foundation of China) 81874192
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is one of the first and most prominent driver genes known to promote malignant lung cancer. Investigating regulatory mechanisms beyond ligand-receptor binding, phosphorylation, and receptor kinase activation as means of EGFR signaling activation is important for improving EGFR-targeted therapy. Here, we report that Laminin-5γ-2 (LAMC2) retained high oncogenic capacity in lung cancer, silencing LAMC2 inhibited EGFR-induced cell proliferation and tumor growth in vivo. Deletion mutation experiments showed that both the EGF-Lam and LamB regions of LAMC2 are necessary for EGFR receptor binding, and that LAMC2 and EGFR were found to co-localize at the endoplasmic reticulum (ER) membrane. In addition, LAMC2 overexpression enhanced EGFR membrane deposition and promoted EGFR transport from the ER. Moreover, LAMC2 was necessary for preventing EGFR protein degradation via ubiquitination. Lastly, our study showed that high LAMC2 expression is positively associated with response to gefitinib (EGFR tyrosine kinase inhibitor) treatment. Overall, our study revealed a new regulatory mechanism of LAMC2 in promoting EGFR protein expression and stability by facilitating ER transport and preventing protein degradation via ubiquitination. Moreover, LAMC2 may serve as a stratifying biomarker for patients suitable for EGFR-TKI treatment.

Indexed as

Lung NeoplasmsBiomarkersCell Line, TumorCell MembraneDrug Resistance, NeoplasmErbB ReceptorsHumansLamininMutationProtein Kinase InhibitorsTyrosine Kinase InhibitorsBiomarkersEGFR protein, humanErbB ReceptorsLAMC2 protein, humanLamininProtein Kinase InhibitorsTyrosine Kinase Inhibitors

Identifiers

PMID37542131
PMCPMC10645587
OpenAlexW4385583463

What OpenQuestion holds

Textmetadata
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.