Evidence map›Paper›PMID 29218238›Full record

ArticleAmerican journal of cancer research2017

MicroRNA-936 induces cell cycle arrest and inhibits glioma cell proliferation by targeting CKS1.

Dong Wang, Tongle Zhi, Xiupeng Xu, Zhongyuan Bao, Liang Fan, Zheng Li, Jing Ji, Ning Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Dong WangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Tongle ZhiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Xiupeng XuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Zhongyuan BaoDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Liang FanDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Zheng LiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Jing JiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Ning LiuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029, Jiangsu Province, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence shows that microRNAs play important roles in cancers, including glioma. MiRNAs have been shown to participate in a variety of cellular functions including cell apoptosis, cell proliferation, neural development, and stem cell differentiation. Previous studies reported that miR-936 levels were downregulated in glioma specimens. Here, we further investigate the potential role of miR-936 in glioma. Quantitative reverse transcription-PCR was applied to detect the expression of mir-936 in glioma specimens. The direct targets of miR-936 were identified by bioinformatics analysis and were further validated by immunoblotting and luciferase reporter assay. The effects of miR-936 on glioma cell proliferation and cell cycle of glioma cells were analyzed by Cell-Counting Kit 8 assay, colony formation, 5-ethynyl-2-deoxyuridine (EDU) and flow cytometry assays. A xenograft model was used to study the effect of miR-936 on tumor growth and angiogenesis. Expression levels of miR-936 were greatly downregulated in glioma specimens, CKS1 was confirmed as a direct target of miR-936. The glioma cell cycle was blocked to G1 by negatively regulating CKS1 and its downstream signaling pathway, Akt-ERK1/2. Furthermore, overexpression of CKS1 rescued the inhibitory effects of miR-936. In vivo studies revealed that increased levels of miR-936 delayed the growth of tumors. Taken together, mir-936 may act as a glioma suppressor by targeting CKS1.

Indexed as

CKS1gliomamiR-936proliferation

Identifiers

PMID29218238
PMCPMC5714743
OpenAlexW2979620396

What OpenQuestion holds

Textmetadata
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.