Evidence map›Paper›PMID 26016795›Full record

ArticleBMC cancer2015

MicroRNA-217 functions as a prognosis predictor and inhibits colorectal cancer cell proliferation and invasion via an AEG-1 dependent mechanism.

Bo Wang, Zhan-Long Shen, Ke-Wei Jiang, Gang Zhao, Chun-You Wang, Yi-Chao Yan, Yang Yang, Ji-Zhun Zhang, Chao Shen, Zhi-Dong Gao and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

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  7. Bladder mesenchymal stromal cell-derived exosomal miRNA-217 modulates bladder cancer cell survival through Hippo-YAP pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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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

12 authors at 3 institutions in 1 country.

Bo WangDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. bowang1986@126.com.
Zhan-Long ShenDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. shenlong1977@163.com.
Ke-Wei JiangDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. jiangkewei@pkuph.edu.cn.
Gang ZhaoPancreatic Disease Institute, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. gangzhao1975@126.com.
Chun-You WangPancreatic Disease Institute, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. chyouwang52@126.com.
Yi-Chao YanDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. yanych0306@126.com.
Yang YangDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. docyang_2013@163.com.
Ji-Zhun ZhangDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. zhangjizhun2007@163.com.
Chao ShenDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. sc201@163.com.
Zhi-Dong GaoDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. gaodong1234567@163.com.
Ying-Jiang YeDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. yeyingjiang@pkuph.edu.cn.
Shan WangDepartment of Gastroenterological Surgery, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, P.R. China. shanwang60@sina.com.
Peking University · CNPeking University People's Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have indicated the possible function of miR-217 in tumorigenesis. However, the roles of miR-217 in colorectal cancer (CRC) are still largely unknown.

methodsWe examined the expression of miR-217 and AEG-1 in 50 CRC tissues and the corresponding noncancerous tissues by qRT-PCR. The clinical significance of miR-217 was analyzed. CRC cell lines with miR-217 upregulation and AEG-1 silencing were established and the effects on tumor growth in vitro and in vivo were assessed. Dual-luciferase reporter gene assays were also performed to investigate the interaction between miR-217 and AEG-1.

resultsOur data demonstrated that miR-217 was significantly downregulated in 50 pairs of colorectal cancer tissues. MiR-217 expression levels were closely correlated with tumor differentiation. Moreover, decreased miR-217 expression was also associated with shorter overall survival of CRC patients. MiR-217 overexpression significantly inhibited proliferation, colony formation and invasiveness of CRC cells by promoting apoptosis and G0/G1 phase arrest. Interestingly, ectopic miR-217 expression decreased AEG-1 expression and repressed luciferase reporter activity associated with the AEG-1 3'-untranslated region (UTR). AEG-1 silencing resulted in similar biological behavior changes to those associated with miR-217 overexpression. Finally, in a nude mouse xenografted tumor model, miR-217 overexpression significantly suppressed CRC cell growth.

conclusionsOur findings suggest that miR-217 has considerable value as a prognostic marker and potential therapeutic target in CRC.

Indexed as

AgedAnimalsApoptosisBiomarkers, TumorCell Adhesion MoleculesCell Cycle CheckpointsCell Line, TumorCell ProliferationCell Transformation, NeoplasticColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsMiceBiomarkers, TumorCell Adhesion MoleculesMembrane ProteinsMicroRNAsMIRN217 microRNA, humanMTDH protein, humanRNA-Binding Proteins

Identifiers

PMID26016795
PMCPMC4446846
OpenAlexW2120256899

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.