Evidence map›Paper›PMID 27924500›Full record

ArticleJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban2016

miR-124 modulates gefitinib resistance through SNAI2 and STAT3 in non-small cell lung cancer.

Fa-Yong Hu, Xiao-Nian Cao, Qin-Zi Xu, Yu Deng, Sen-Yan Lai, Jing Ma, Jun-Bo Hu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 26 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

7 authors at 2 institutions in 1 country.

Fa-Yong HuCancer Research Institute, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiao-Nian CaoDepartment of Thoracic Surgery, Huazhong University of Science and Technology, Wuhan, 430030, China.
Qin-Zi XuDepartment of Thoracic Surgery, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yu DengDepartment of Thoracic Surgery, Huazhong University of Science and Technology, Wuhan, 430030, China.
Sen-Yan LaiCancer Research Institute, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jing MaDepartment of Respiratory and Critical Care Medicine, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jun-Bo HuCancer Research Institute, Huazhong University of Science and Technology, Wuhan, 430030, China. jbhu@tjh.tjmu.edu.cn.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gefitinib is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). Unfortunately, most NSCLC patients inevitably develop gefitinib resistance during treatment. In addition to EGFR mutation status, the mechanisms involved are largely unknown. In this study, we showed that miR-124, a tumor suppressor, was significantly down-regulated in gefitinib-resistant NSCLC patients and cell lines compared with gefitinib-sensitive patients and cell lines. In addition, the miR-124 depletion induced gefitinib resistance, and miR-124 overexpression sensitized gefitinib-resistant cells to gefitinib. Mechanistic analysis revealed that miR-124 decreased SNAI2 and STAT3 expression by directly targeting their 3'UTRs and that knocking down SNAI2 or STAT3 partly reversed the gefitinib resistance induced by miR-124 depletion. Our data demonstrate that the miR-124 plays a new critical role in acquired resistance to gefitinib and that the manipulation of miR-124 might provide a therapeutic strategy for reversing acquired gefitinib resistance.

Indexed as

3' Untranslated RegionsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorDrug Resistance, NeoplasmGefitinibHEK293 CellsHumansLung NeoplasmsMicroRNAsQuinazolinesSnail Family Transcription FactorsSTAT3 Transcription Factor3' Untranslated RegionsAntineoplastic AgentsGefitinibMicroRNAsMIRN124 microRNA, humanQuinazolinesSNAI2 protein, humanSnail Family Transcription FactorsSTAT3 protein, humanSTAT3 Transcription Factorgefitinib-resistancemiR-124non-small cell lung cancerSNAI2STAT3

Identifiers

PMID27924500
OpenAlexW2572540760

What OpenQuestion holds

Textmetadata
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.