Evidence map›Paper›PMID 30816202›Full record

ArticleScientific reports2019

MiR-494 acts as a tumor promoter by targeting CASP2 in non-small cell lung cancer.

Qiao Zhang, Yan Li, Mei Zhao, Hong Lin, Wenjie Wang, Dongdong Li, Wei Cui, Caihong Zhou, Jialing Zhong, Changzhi Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  9. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
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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 2 institutions in 1 country.

Qiao ZhangDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Yan LiDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Mei ZhaoDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Hong LinDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Wenjie WangDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Dongdong LiDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Wei CuiDepartment of Clinical Laboratory, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Caihong ZhouDepartment of Education, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Jialing ZhongClinical Laboratory, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China. zhongjl03@163.com.
Changzhi HuangDepartment of Etiology and Carcinogenesis, State Key Laboratory of Molecular Oncology, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. huangpumc@163.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-494 plays an important role in several types of human cancers, including non-small cell lung cancer (NSCLC). Although the role of miR-494 has been investigated in several studies, the expression profile and underlying mechanism are still poorly understood. In this study, we found that overexpression of miR-494 promoted the proliferation and colony formation of NSCLC cells and reduced their sensitivity to cisplatin-induced apoptosis. By using microarray and Dual luciferase reporter assays, we further showed that caspase-2 (CASP2) is a functional target of miR-494, and the expression of CASP2 is inversely associated with miR-494 in vitro. In addition, miR-494 promoted the proliferation and colony formation of NSCLC cells and reduced their sensitivity to cisplatin-induced apoptosis by targeting CASP2. Therefore, our results suggest that miR-494 plays an oncomiR role in NSCLC cells and may be a candidate biomarker for malignant transformation and a therapeutic target of NSCLC.

Indexed as

A549 CellsAntineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCaspase 2Cell ProliferationCisplatinCysteine EndopeptidasesGene Expression Regulation, NeoplasticHEK293 CellsHumansLung NeoplasmsMicroRNAsAntineoplastic AgentsCASP2 protein, humanCaspase 2CisplatinCysteine EndopeptidasesMicroRNAsMIRN494 microRNA, human

Identifiers

PMID30816202
PMCPMC6395740
OpenAlexW2920406367

What OpenQuestion holds

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LicenceCC BY
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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.