Evidence map›Paper›PMID 25628794›Full record

ArticleAmerican journal of translational research2014

MiR-223 suppresses endometrial carcinoma cells proliferation by targeting IGF-1R.

Kai Huang, Xiyuan Dong, Cong Sui, Dan Hu, Ting Xiong, Shujie Liao, Hanwang Zhang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  5. Non-Coding RNAs as Prognostic Markers for Endometrial Cancer.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Bta-miR-223 Targeting CBLB Contributes to Resistance toFrontiers in veterinary science · 2020
    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

7 authors at 1 institution in 1 country.

Kai HuangReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Xiyuan DongReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Cong SuiReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Dan HuReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Ting XiongReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Shujie LiaoReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Hanwang ZhangReproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, The People's Republic of China.
Tongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs were recently found to participate in oncogenesis and growth of various tumors. We hypothesized that microRNA-223 (miR-223) plays a role in endometrial carcinoma growth. In this study, we transfected RL95-2 cells with lentivirus containing miR-223 precursor to establish a miR-223 over-expression model. Proliferation of the cells was greatly inhibited when miR-223 was over-expressed, and cell cycle progress was blocked in G0/G1 phase. To investigate the mechanisms involved, we scanned the putative target genes of miR-223 using bioinformatics, and confirmed that insulin-like growth factor-1 receptor (IGF-1R) was a functional target of miR-223 using quantitative PCR, Western blot and luciferase reporter assay. Meanwhile, over-expressed miR-223 was found to regulate the expression of IGF-1R by repressing protein translation. Silencing IGF-1R with small interfering RNA resulted in similar effect as miR-223 overexpression. Therefore, our data suggest that miR-223 regulates RL95-2 cells proliferation and cell cycle progress by targeting IGF-1R.

Indexed as

cell proliferationendometrial carcinoma cellinsulin-like growth factor-1 receptorin vitroMiR-223

Identifiers

PMID25628794
PMCPMC4297351
OpenAlexW115814958

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.