Evidence map›Paper›PMID 22207524›Full record

ArticleJournal of cancer research and clinical oncology2012

MiR-181d acts as a tumor suppressor in glioma by targeting K-ras and Bcl-2.

Xie-Feng Wang, Zhu-Mei Shi, Xi-Rui Wang, Lei Cao, Ying-Yi Wang, Jun-Xia Zhang, Yu Yin, Hui Luo, Chun-Sheng Kang, Ning Liu and 2 more

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Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing 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

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

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  9. The Role of RAS in CNS Tumors: A Key Player or an Overlooked Oncogene?International journal of molecular sciences · 2025
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16 more citing papers are in PubMed but not listed here.

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

12 authors.

Xie-Feng WangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, Jiangsu Province, People's Republic of China.
Zhu-Mei Shi
Xi-Rui Wang
Lei Cao
Ying-Yi Wang
Jun-Xia Zhang
Yu Yin
Hui Luo
Chun-Sheng Kang
Ning Liu
Tao Jiang
Yong-Ping You

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRecently, several microRNAs (miRNAs) were reported to be involved in the modulation of glioma development. The aim of our study was to determine the effect of miR-181d on the growth of glioma and to investigate whether this growth is modulated by targeting K-ras and Bcl-2.

methodsReal-time PCR was used to analyze the expression of miR-181d in human glioma samples and glioma cell lines. Apoptosis, cell cycle, and proliferation (MTT) assays were performed to assess the phenotypic changes in glioma cells. Immunohistochemistry was used to determine the expression of K-ras and Bcl-2 in glioma tissues, and a luciferase reporter assay was carried out to confirm whether K-ras and Bcl-2 are direct targets of miR-181d. Western blotting was used to identify the potential signaling pathways affected glioma cell growth by miR-181d. In vivo, xenograft tumors were examined for an anti-glioma effect of miR-181d.

resultsMiR-181d was down-regulated in human glioma samples and up-regulated in transfected glioma cells. Ectopic expression of miR-181d suppressed proliferation and triggered cell cycle arrest and apoptosis in glioma cell lines. K-ras and Bcl-2 were identified as direct targets of miR-181d and were up-regulated in glioma samples. The results showed evidence linking the tumor suppressor activity of miR-181d in glioma cells with the K-ras-related PI3K/AKT and MAPK/ERK pathways. Furthermore, xenograft tumors from miR-181d-treated U251 cells were suppressed in vivo.

conclusionMiR-181d may act as a glioma suppressor by targeting K-ras and Bcl-2.

Indexed as

Genes, Tumor Suppressor3' Untranslated RegionsAnimalsApoptosisBase SequenceBinding SitesBlotting, WesternBrainCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGliomaHumansImmunohistochemistryMice3' Untranslated RegionsMicroRNAsMIrn181 microRNA, humanMitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins p21(ras)

Identifiers

PMID22207524
PMCPMC11824363

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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.