Evidence map›Paper›PMID 27121316›Full record

ArticleOncotarget2016

Epigenetic modification of miR-141 regulates SKA2 by an endogenous 'sponge' HOTAIR in glioma.

Er-Bao Bian, Chun-Chun Ma, Xiao-Jun He, Chao Wang, Gang Zong, Hong-Liang Wang, Bing Zhao

Open access · diamondAbstract read
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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.9field-weighted citation impact, top 6% 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, 68 citations in OpenAlex.

  1. Review
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  4. The multifaceted functions of long non-coding RNAExpert reviews in molecular medicine · 2024
    Review
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  18. Article
  19. Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  20. HOX Transcript Antisense RNANon-coding RNA · 2020
    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

7 authors at 2 institutions in 1 country.

Er-Bao BianDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Chun-Chun MaDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Xiao-Jun HeDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Chao WangDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Gang ZongDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Hong-Liang WangDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Bing ZhaoDepartment of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, 230601, Hefei, China.
Second Hospital of Anhui Medical University · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant expression of miR-141 has recently implicated in the occurrence and development of various types of malignant tumors. However whether the involvement of miR-141 in the pathogenesis of glioma remains unknown. Here, we showed that miR-141 was markedly downregulated in glioma tissues and cell lines compared with normal brain tissues, and its expression correlated with the pathological grading. Enforced expression of miR-141 in glioma cells significantly inhibited cell proliferation, migration and invasion, whereas knockdown of miR-141 exerted opposite effect. Mechanistic investigations revealed that HOTAIR might act as an endogenous 'sponge' of miR-141, thereby regulating the derepression of SKA2. Further, we explored the molecular mechanism by which miR-141 expression was regulated, and found that the miR-141 promoter was hypermethylated and that promoter methylation of miR-141 was mediated by DNMT1 in glioma cells. Finally, both overexpression of miR-141 and knockdown of HOTAIR in a mouse model of human glioma resulted in significant reduction of tumor growth in vivo. Collectively, these results suggest that epigenetic modification of miR-141 and the interaction of ceRNA regulatory network will provide a new approach for therapeutics against glioma.

Indexed as

DNA Methylation3' Untranslated RegionsAnimalsBrain NeoplasmsCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneFemaleGene Expression Regulation, NeoplasticGliomaHumansMice, Inbred BALB CMice, NudeMicroRNAsPromoter Regions, GeneticRNA, Long Noncoding3' Untranslated RegionsChromosomal Proteins, Non-HistoneHOTAIR long untranslated RNA, humanMicroRNAsMIRN141 microRNA, humanRNA, Long NoncodingSKA2 protein, humanDNMT1gliomasHOTAIRmiR-141SKA2

Identifiers

PMID27121316
PMCPMC5058705
OpenAlexW2340764667

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.