Evidence map›Paper›PMID 29970127›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

CPNE1 is a target of miR-335-5p and plays an important role in the pathogenesis of non-small cell lung cancer.

Haicheng Tang, Jianjie Zhu, Wenwen Du, Shunlin Liu, Yuanyuan Zeng, Zongli Ding, Yang Zhang, Xueting Wang, Zeyi Liu, Jianan Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

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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 at 3 institutions in 1 country.

Haicheng TangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Jianjie ZhuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Wenwen DuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Shunlin LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Yuanyuan ZengDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Zongli DingDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Yang ZhangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Xueting WangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Zeyi LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China. liuzeyisuda@163.com.
Jianan HuangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China. huang_jian_an@163.com.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNSuzhou Research Institute · CN

Funding

Clinical Medical Center of Suzhou Szzx201502Jiangsu Provincial Key Medical Discipline ZDXKB2016007Jiangsu Provincial Medical Youth Talent QNRC2016746National Natural Science Foundation of China 81201575Science and Technology Plan Projects of Suzhou SYS201612Suzhou Key Laboratory for Respiratory Medicine SZS201617
6 · The paper itself

Abstract

backgroundDespite advances in diagnosis and treatment, the survival of non-small cell lung cancer (NSCLC) patients remains poor. There is therefore a strong need to identify potential molecular targets for the treatment of NSCLC. In the present study, we investigated the function of CPNE1 in the regulation of cell growth, migration and invasion.

methodsQuantitative real-time PCR (qRT-PCR) was used to detect the expression of CPNE1 and miR-335-5p. Western blot and immunohistochemical assays were used to investigate the levels of CPNE1 and other proteins. Flow cytometry was used to determine cell cycle stage and apoptosis. CCK-8 and clonogenic assays were used to investigate cell proliferation. Wound healing, migration and invasion assays were used to investigate the motility of cells. A lung carcinoma xenograft mouse model was used to investigate the in vivo effects of CPNE1 overexpression.

resultsWe observed that knockdown of CPNE1 and increased expression of miR-335-5p inhibits cell proliferation and motility in NSCLC cells, and found that CPNE1 was a target of miR-335-5p. In addition, our data indicated that CPNE1 inhibition could improve the clinical effects of EGFR-tyrosine kinase inhibitors.

conclusionsThe present results indicate that CPNE1 may be a promising molecular target in the treatment of NSCLC.

Indexed as

Gene Expression Regulation, NeoplasticAgedAged, 80 and overAnimalsApoptosisCalcium-Binding ProteinsCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleHeterograftsHumansIncidenceCalcium-Binding ProteinsCPNE1 protein, humanMicroRNAsMIRN335 microRNA, humanCopine 1 (CPNE1)microRNAmiR-335-5pNon-small cell lung cancer (NSCLC)

Identifiers

PMID29970127
PMCPMC6029376
OpenAlexW2811229930

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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.