Evidence map›Paper›PMID 27012554›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

MicroRNA-134 modulates glioma cell U251 proliferation and invasion by targeting KRAS and suppressing the ERK pathway.

Yuguang Zhao, Dong Pang, Cui Wang, Shijiang Zhong, Shuang Wang

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Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  6. Article
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  11. Review
  12. miR-134: A Human Cancer Suppressor?Molecular therapy. Nucleic acids · 2017
    Review
  13. Article
  14. MiR-124 inhibits cell proliferation, invasion, and migration in glioma by targeting Smad2.International journal of clinical and experimental pathology · 2017
    Article
  15. Article
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

5 authors at 4 institutions in 1 country.

Yuguang ZhaoDepartment of Cell Biology, Harbin Medical University, Harbin, 150081, China.
Dong PangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, No. 248 Xuefu Road, Nangang District, Harbin, 150086, China.
Cui WangLand Reclamation of Community Health Service Stations, General Hospital of Heilongjiang Agricultural Reclamation Bureau, Harbin, 150090, China.
Shijiang ZhongDepartment of Brain, The Affiliated Hospital of Tianjin Armed Police College, Tianjin, 300163, China.
Shuang WangDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, No. 248 Xuefu Road, Nangang District, Harbin, 150086, China. shuangw_hmu@126.com.
Harbin Medical University · CNChinese People's Armed Police Force Medical College Affiliated Hospital · CNHeilongjiang Academy of Land Reclamation Sciences · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated microRNA-134 (miR-134) has been observed in glioma carcinogenesis, and studies suggested that the ERK pathway plays vital roles in glioma cell growth and proliferation. However, the fundamental relationship between miR-134 and the ERK pathway in glioma has not been fully explained. As a result, this study was aimed to explore the underlying functions of miR-134 in human glioma. Intentionally overexpressed or inhibited miR-134 expression resulted from the transfection of miR-134 mimics, or miR-134 inhibitor within glioma cell line U251 was detected using RT-PCR. Both cell counting kit-8 (CCK-8) assays and Transwell assays were carried out to clarify the proliferation and invasion of U251 cells transfected with miR-134 mimics or miR-134 inhibitors. Our findings showed that miR-134 was significantly downexpressed in glioma tissues, and low miR-134 expression was significantly related to high histopathological grades. However, upregulated miR-134 expression restrained the proliferation and invasion of U251 cells in vitro. Kirsten rat sarcoma viral oncogene (KRAS), a vital factor for the ERK pathway, was directly targeted by miR-134 through its binding with the 3'-UTR of KRAS in glioma. Furthermore, KRAS expression exhibited a positive correlation with the activity of the ERK pathway. Overexpression of KRAS without 3'-UTR partly offsets the suppressive effect of miR-134 on glioma progression. Our data also indicated that miR-134 negatively modulated glioma progression and upregulated miR-134 triggered aberrant activation of the ERK pathway by targeting KRAS. Therefore, miR-134 might be considered as a benign therapeutic target of glioma.

Indexed as

AdultAgedAged, 80 and overBlotting, WesternBrain NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGliomaHumansImmunohistochemistryMaleMAP Kinase Signaling SystemMicroRNAsMiddle AgedKRAS protein, humanMicroRNAsMIRN134 microRNA, humanProto-Oncogene Proteins p21(ras)ERK pathwayGliomaInvasionKRASMicroRNA-134Proliferation

Identifiers

PMID27012554
OpenAlexW2306091558

What OpenQuestion holds

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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.