Evidence map›Paper›PMID 35013118›Full record

ArticleCell death & disease2022

Neurokinin-1 receptor promotes non-small cell lung cancer progression through transactivation of EGFR.

Xiao-Wei Zhang, Lin Li, Wen-Qian Hu, Ming-Ning Hu, Yan Tao, Hui Hu, Xiao-Kang Miao, Wen-Le Yang, Qiong Zhu, Ling-Yun Mou

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 49 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Xiao-Wei ZhangSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Lin LiSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Wen-Qian HuSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Ming-Ning HuSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Yan TaoKey Laboratory of Urological Disease of Gansu Province, Lanzhou University Second Hospital, Lanzhou University, Lanzhou, 730000, P. R. China.
Hui HuSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Xiao-Kang MiaoBasic Medical Sciences & Research Unit of Peptide Science, Chinese Academy of Medical Sciences, 2019RU066, Lanzhou University, Lanzhou, 730000, P. R. China.
Wen-Le YangBasic Medical Sciences & Research Unit of Peptide Science, Chinese Academy of Medical Sciences, 2019RU066, Lanzhou University, Lanzhou, 730000, P. R. China.
Qiong ZhuSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China.
Ling-Yun MouSchool of Life Science Lanzhou University, 222 TianShui South Road, Lanzhou, 730000, P. R. China. muly@lzu.edu.cn.ORCID http://orcid.org/0000-0002-1328-5776
Chinese Academy of Medical Sciences & Peking Union Medical College · CNLanzhou University · CNLanzhou University Second Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the great advances in target therapy, lung cancer remains the top cause of cancer-related death worldwide. G protein-coupled receptor neurokinin-1 (NK1R) is shown to play multiple roles in various cancers; however, the pathological roles and clinical implication in lung cancer are unclarified. Here we identified NK1R as a significantly upregulated GPCR in the transcriptome and tissue array of human lung cancer samples, associated with advanced clinical stages and poor prognosis. Notably, NK1R is co-expressed with epidermal growth factor receptor (EGFR) in NSCLC patients' tissues and co-localized in the tumor cells. NK1R can crosstalk with EGFR by interacting with EGFR, transactivating EGFR phosphorylation and regulating the intracellular signaling of ERK1/2 and Akt. Activation of NK1R promotes the proliferation, colony formation, EMT, MMP2/14 expression, and migration of lung cancer cells. The inhibition of NK1R by selective antagonist aprepitant repressed cell proliferation and migration in vitro. Knockdown of NK1R significantly slowed down the tumor growth in nude mice. The sensitivity of lung cancer cells to gefitinib/osimertinib is highly increased in the presence of the selective NK1R antagonist aprepitant. Our data suggest that NK1R plays an important role in lung cancer development through EGFR signaling and the crosstalk between NK1R and EGFR may provide a potential therapeutic target for lung cancer treatment.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationDisease ProgressionDrug SynergismErbB ReceptorsHumansLung NeoplasmsMiceNeurokinin-1 Receptor AntagonistsPhosphorylationPrognosisProtein Kinase InhibitorsReceptors, Neurokinin-1EGFR protein, humanErbB ReceptorsNeurokinin-1 Receptor AntagonistsProtein Kinase InhibitorsReceptors, Neurokinin-1TACR1 protein, human

Identifiers

PMID35013118
PMCPMC8748918
OpenAlexW4206752633

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.