Evidence map›Paper›PMID 26832151›Full record

ArticleMolecular cancer2016

MicroRNA-505 functions as a tumor suppressor in endometrial cancer by targeting TGF-α.

Shuo Chen, Kai-Xuan Sun, Bo-Liang Liu, Zhi-Hong Zong, Yang Zhao

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
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  7. Article
  8. Article
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  13. Review
  14. Non-Coding RNAs as Prognostic Markers for Endometrial Cancer.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Article
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  18. Observational
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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

5 authors at 2 institutions in 1 country.

Shuo ChenDepartment of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Kai-Xuan SunDepartment of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Bo-Liang LiuDepartment of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Zhi-Hong ZongDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, Shenyang, 100013, China.
Yang ZhaoDepartment of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China. yida.zhaoyang@163.com.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndometrial carcinoma (EC) is one of the most lethal gynecologic cancers. Patients frequently have regional or distant metastasis at diagnosis. MicroRNAs are small non-coding RNAs that participate in numerous biological processes. Recent studies have demonstrated that miR-505 is associated with several types of cancer; however, the expression and function of miR-505 have not been investigated in EC.

methodsmiR-505 expression in normal endometrial tissue, endometrial carcinomas were quantified by Quantitative reverse transcription PCR. The endometrial carcinoma cell lines HEC-1B and Ishikawa were each transfected with miR-505 or scrambled mimics, after which cell phenotype and expression of relevant molecules were assayed. Dual-luciferase reporter assay and a xenograft mouse model were used to examine miR-505 and its target gene TGF-α.

resultsRT-PCR results demonstrated that miR-505 was significantly downregulated in human EC tissues compared to normal endometrial tissues. Besides, miR-505 expression was negatively associated with FIGO stage (stage I-II vs. III-IV), and lymph node metastasis (negative vs. positive). In vitro, overexpression of miR-505 significantly suppressed EC cell proliferation, increased apoptosis and reduced migratory and invasive activity. A miR-505 binding site was identified in the 3' untranslated region of TGF-α mRNA (TGFA) using miRNA target-detecting software; a dual luciferase reporter assay confirmed that miR-505 directly targets and regulates TGFA. RT-PCR and Western-blotting results indicated that overexpressing miR-505 reduced the expression of TGF-α and the TGF-α-regulated proteins MMP2, MMP9, CDK2, while induced Bax and cleaved-PARP expression in EC cells. In vivo, overexpression of miR-505 reduced the tumorigenicity and inhibited the growth of xenograft tumors in a mouse model of EC.

conclusionsTaken together, this study demonstrates that miR-505 acts as tumor suppressor in EC by regulating TGF-α.

Indexed as

Genes, Tumor SuppressorAnimalsApoptosisBase SequenceCarcinogenesisCell Line, TumorCell ProliferationDisease Models, AnimalEndometrial NeoplasmsFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMicroRNAsMolecular Sequence DataMicroRNAsMIRN505 microRNA, humanTransforming Growth Factor alpha

Identifiers

PMID26832151
PMCPMC4736705
OpenAlexW2271267346

What OpenQuestion holds

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LicenceCC BY
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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.