Evidence map›Paper›PMID 41190648›Full record

ArticleJournal of cellular and molecular medicine2025

Targeting MET Signalling Activated by CPNE3-RACK1 Interaction Through VWFA Domain to Suppress Lung Cancer Progression.

Xin Cai, Jian Zhao, Chenkang Ma, Min Jiao, Weijie Zhang, Anqi Wang, Jianjun Li, Jianjie Zhu, Yuanyuan Zeng, Chuanyong Mu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. 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

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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. Article
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

12 authors.

Xin CaiDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jian ZhaoDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Chenkang MaDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Min JiaoDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Weijie ZhangDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Anqi WangDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jianjun LiDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jianjie ZhuDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Yuanyuan ZengDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-2260-4468
Chuanyong MuDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Jian-An HuangDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.
Zeyi LiuDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-2528-6909

Funding

Jiangsu Provincial Medical Key Discipline ZDXK202201National Natural Science Foundation of China 82273150Original Exploration program for Suzhou Basic Research SSD2024024Original Exploration program for Suzhou Basic Research SSD2024036Original Exploration program for Suzhou Basic Research SSD2024096The 6th "333 High-level Talents Training Project" of Jiangsu Province 2022-3-25-162
6 · The paper itself

Abstract

Despite advances in diagnosis and treatment, the prognosis of non-small cell lung cancer (NSCLC) remains poor. Therefore, it is urgent to identify potential molecular targets. In this study, we investigated the function and internal mechanism of CPNE3 in the malignant biological behaviour via RACK1/c-MET signalling in NSCLC, and explored the feasibility of the MET inhibitor in NSCLC treatment. The expression of CPNE3 in normal tissues and lung cancer tissues was compared using a public database. The function of CPNE3 was investigated using CCK-8 assays, clonogenic assays, EdU assays, Transwell assays and cell cycle analysis. Western blotting was used to detect the protein expression. The interaction between CPNE3 and RACK1 was examined by immunofluorescence staining and co-immunoprecipitation (co-IP). The in vitro and in vivo functions of the MET inhibitor JNJ-38877605 were investigated. CPNE3 is overexpressed in NSCLC and facilitates tumorigenesis and metastasis by interacting with RACK1 through the VWFA domain, which further induces the activation of MET signalling. Accordingly, this process could be suppressed by the MET inhibitor and RACK1 knockdown in vitro and in vivo. CPNE3 is highly expressed in NSCLC and can promote the proliferation and migration of tumour cells. CPNE3 could interact with RACK1 through the VWFA domain and activate MET signalling. These findings may provide new insights into the development of novel therapeutic strategies for NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsNeoplasm ProteinsProto-Oncogene Proteins c-metReceptors for Activated C KinaseSignal TransductionAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeMET protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-metRACK1 protein, humanReceptors for Activated C KinaseCPNE3JNJ‐38877605METNSCLCRACK1

Identifiers

PMID41190648
PMCPMC12587306

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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.