Evidence map›Paper›PMID 27083050›Full record

ArticleOncotarget2016

Reduction of microRNA-184 by E6 oncoprotein confers cisplatin resistance in lung cancer via increasing Bcl-2.

Min-Che Tung, Po-Lin Lin, Ya-Wen Cheng, De-Wei Wu, Sauh-Der Yeh, Chi-Yi Chen, Huei Lee

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  12. The Roles of MicroRNA in Lung Cancer.International journal of molecular sciences · 2019
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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.

Min-Che TungGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
Po-Lin LinInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Ya-Wen ChengGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
De-Wei WuGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
Sauh-Der YehGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
Chi-Yi ChenDepartment of Surgery, Chung Shan Medical University, Taichung, Taiwan.
Huei LeeGraduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-184 suppresses cell growth and survival via targeting c-Myc and Bcl- 2. We recently reported that miR-184 promotes tumor progression in non-small cell lung cancer via targeting CDC25A and c-Myc. We here hypothesized that miR-184 could be down-regulated by E6 oncoprotein to confer cisplatin resistance in NSCLC. Human papillomavirus (HPV) 16-positive lung cancer TL-1 and cervical cancer SiHa cells compared with HPV16-negative TL-10 and C33A cells were enrolled for E6 manipulation. MiR-184 expression levels were increased by E6-knockdown in TL-1 and SiHa cells, but decreased by E6-overexpression in TL-10 and C33A cells. The MTT assay showed that the inhibition concentration of cisplatin yielding for 50% cell viability was dependent on miR-184 levels. Bcl-2 de-targeted by E6-mediated miR- 184 reduction was responsible for cisplatin resistance. Luciferase reporter assay and real- time PCR analysis indicated that the miR-184 promoter activity and its expression were modulated by E6 and/or p53 manipulation. Chromatin immunoprecipitation (ChIP) assay confirmed that p53 was bound onto the miR-184 promoter and its binding activity was modulated by E6 and/or p53 manipulation. Among patients, high miR184 and high Bcl-2 mRNA expression was more commonly occurred in E6- positive tumors than in E6-negative tumors. Fifty-nine out of 136 patients receiving cisplatin-based chemotherapy were available for the retrospective study. Patients with low-mR-184, E6-positive, high-Bcl-2 tumors, and both combinations were more prevalently occurred unfavorable response to cisplatin-based chemotherapy than their counterparts. In conclusion, a decrease in miR-184 level by E6 oncoprotein may predict unfavorable response to cisplatin-based chemotherapy in HPV-infected NSCLC patients via increasing Bcl-2 expression.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsBinding SitesCarcinoma, Non-Small-Cell LungCell Line, TumorCell SurvivalCisplatinDose-Response Relationship, DrugGene Expression Regulation, NeoplasticHuman papillomavirus 16HumansLung NeoplasmsMicroRNAsOncogene Proteins, ViralPapillomavirus InfectionsPromoter Regions, GeneticAntineoplastic AgentsBCL2 protein, humanCisplatinE6 protein, Human papillomavirus type 16MicroRNAsMIRN184 microRNA, humanOncogene Proteins, ViralProto-Oncogene Proteins c-bcl-2Repressor ProteinsTP53 protein, humanTumor Suppressor Protein p53cisplatin resistanceHPVmiR-184

Identifiers

PMID27083050
PMCPMC5078019

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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.