Evidence map›Paper›PMID 26593208›Full record

ArticleScientific reports2015

Oncogenic miR-9 is a target of erlotinib in NSCLCs.

Xi Chen, Lingjun Zhu, Zhuo Ma, Geng Sun, Xuan Luo, Min Li, Sulan Zhai, Ping Li, Xuerong Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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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

9 authors at 2 institutions in 1 country.

Xi ChenDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Lingjun ZhuDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Zhuo MaDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Geng SunDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Xuan LuoDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Min LiDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Sulan ZhaiDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Ping LiDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Xuerong WangDepartment of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu Province, China, 210029.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EGFR-targeted cancer therapy is a breakthrough in non-small cell carcinoma. miRNAs have been proved to play important roles in cancer. Currently, for the role of miRNAs in EGFR-targeted cancer therapy is unclear. In this study, first we found that erlotinib reduced the expression of miR-9. MiR-9 expression was increased in human lung cancer tissues compared with peripheral normal tissues, and miR-9 promoted the growth of NSCLC cells. Overexpression of miR-9 decreased the growth inhibitory effect of erlotinib. Second, miR-9 decreased FoxO1 expression by directly inhibition of its mRNA translation. Adenovirus-mediated overexpression of FoxO1 or siRNA-mediated downregulation of FoxO1 negatively regulated cell growth. And exogenous overexpression FoxO1 reduced the pro-growth effect of miR-9. Finally, we found that erlotinib upregulated FoxO1 protein expression. Moreover, overexpression of miR-9 decreased erlotinib-induced FoxO1 expression, and overexpression of FoxO1 enhanced the growth inhibitory effects of erlotinib. Additionally, we found that erlotinib downregulates miR-9 expression through suppressing the transcrption of miR-9-1 and enhanced DNA methylation maybe involved. These findings suggest that oncogenic miR-9 targeted FoxO1 to promote cell growth, and downregulation of this axis was involved in erlotinib's growth inhibitory effects. Clarifying the regulation of miRNAs by erlotinib may indicate novel strategies for enhancing EGFR-targeted cancer therapy.

Indexed as

Antineoplastic AgentsBase SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDNA MethylationDrug Resistance, NeoplasmErlotinib HydrochlorideForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansLungLung NeoplasmsMicroRNAsMolecular Sequence DataAntineoplastic AgentsErlotinib HydrochlorideForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanMicroRNAsMIRN92 microRNA, humanProtein Kinase InhibitorsRNA, MessengerRNA, Small Interfering

Identifiers

PMID26593208
PMCPMC4655475
OpenAlexW2404927328

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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.