Evidence map›Paper›PMID 38961814›Full record

ArticleActa biochimica et biophysica Sinica2024

CCL2 promotes EGFR-TKIs resistance in non-small cell lung cancer via the AKT-EMT pathway.

Yunlian Diao, Shibo Huang, Fangpeng Liu, Shu Liao, Chenxi Guan, Xiaojian Xiong, Ping Zhang, Junyao Li, Wei Zhang, Ying Ying

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. 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

10 authors.

Yunlian DiaoJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Shibo HuangThe Clinical Trial Research Center, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Fangpeng LiuJiangxi Provincial Key Laboratory of Respiratory Diseases, Jiangxi Institute of Respiratory Disease, Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Shu LiaoJiangxi Provincial Key Laboratory of Respiratory Diseases, Jiangxi Institute of Respiratory Disease, Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Chenxi GuanDepartment of Physiology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Xiaojian XiongJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Ping ZhangJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Junyao LiJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Wei ZhangJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Ying YingJiangxi Provincial Key Laboratory of Prevention and Treatment of Infectious Diseases, Jiangxi Medical Center for Major Public Health Events, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs) represents a primary cause of treatment failure in non-small cell lung cancer (NSCLC) patients. Chemokine (C-C motif) ligand 2 (CCL2) is recently found to play a pivotal role in determining anti-cancer treatment response. However, the role and mechanism of CCL2 in the development of EGFR-TKIs resistance have not been fully elucidated. In the present study, we focus on the function of CCL2 in the development of acquired resistance to EGFR-TKIs in NSCLC cells. Our results show that CCL2 is aberrantly upregulated in EGFR-TKIs-resistant NSCLC cells and that CCL2 overexpression significantly diminishes sensitivity to EGFR-TKIs. Conversely, CCL2 suppression by CCL2 synthesis inhibitor, bindarit, or

Indexed as

Carcinoma, Non-Small-Cell LungChemokine CCL2Drug Resistance, NeoplasmErbB ReceptorsLung NeoplasmsProtein Kinase InhibitorsSignal TransductionCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansProto-Oncogene Proteins c-aktCCL2 protein, humanChemokine CCL2EGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktCCL2EGFR-TKIs resistanceepithelial-mesenchymal transitionnon-small cell lung cancer

Identifiers

PMID38961814
PMCPMC11532253

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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.