Evidence map›Paper›PMID 24404152›Full record

ArticlePloS one2014

Disturbing miR-182 and -381 inhibits BRD7 transcription and glioma growth by directly targeting LRRC4.

Hailin Tang, Zeyou Wang, Qing Liu, Xiaoping Liu, Minghua Wu, Guiyuan Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  12. MiR-381 functions as a tumor suppressor in gastric cancer by targeting ROCK2.International journal of clinical and experimental pathology · 2019
    Article
  13. Article
  14. Article
  15. MicroRNA-381 inhibits the metastasis of gastric cancer by targeting TMEM16A expression.Journal of experimental & clinical cancer research : CR · 2017
    Article
  16. Downregulation of miR-381 is associated with poor prognosis in papillary thyroid carcinoma.International journal of clinical and experimental pathology · 2017
    Article
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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

6 authors at 3 institutions in 1 country.

Hailin TangCancer Research Institute, Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China ; Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Zeyou WangCancer Research Institute, Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China.
Qing LiuThe Center for Skull Base Surgery and Neurooncology, Hunan Province, Changsha, China.
Xiaoping LiuCancer Research Institute, Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China ; Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Minghua WuCancer Research Institute, Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China ; The Center for Skull Base Surgery and Neurooncology, Hunan Province, Changsha, China.
Guiyuan LiCancer Research Institute, Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha, China.
Central South University · CNMinistry of Education of the People's Republic of China · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inactivated LRRC4 has been clinically detected in gliomas, and promoter hypermethylation has been implicated as the mechanism of inactivation in some of those tumors. Our previous researches indicated that LRRC4 is a target gene of miR-381, the interaction of miR-381 and LRRC4 is involved in glioma growth. In this study, we demonstrate that LRRC4 is a target gene of the other microRNA, miR-182. We found that the high expression of miR-182 and miR-381 in gliomas are involved in pathological malignant progression. The silencing of miR-182 and miR-381 inhibited the proliferation in vitro and growth of glioma cell with in vivo magnetic resonance imaging by intracranial transplanted tumor model in rats. We also demonstrated that BRD7, a transcriptional cofactor for p53, is highly expressed and negatively correlated with LRRC4 expression in gliomas. Disturbing miR-182 and miR-381 affected transcriptional regulation of the BRD7 gene. This finding was verified by ectopic overexpression of LRRC4 or restoration of endogenous LRRC4 expression by treatment with the DNA demethylating agent 5-Aza-dC. Taken together, miR-182 and miR-381 may be a useful therapeutic target for treatment of glioma.

Indexed as

Transcription, GeneticAnimalsBase PairingBase SequenceBromodomain Containing ProteinsCell Line, TumorCell Transformation, NeoplasticChromosomal Proteins, Non-HistoneDisease Models, AnimalGene Expression Regulation, NeoplasticGene SilencingGliomaHeterograftsHumansMicroRNAsNerve Tissue ProteinsBRD7 protein, humanBromodomain Containing ProteinsChromosomal Proteins, Non-HistoneLRRC4 protein, humanMicroRNAsMirn182 microRNA, humanMIRN381 microRNA, humanNerve Tissue Proteins

Identifiers

PMID24404152
PMCPMC3880275
OpenAlexW2015314200

What OpenQuestion holds

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LicenceCC BY
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.