Evidence map›Paper›PMID 22754369›Full record

ArticleInternational journal of molecular sciences2012

Revealing the anti-tumor effect of artificial miRNA p-27-5p on human breast carcinoma cell line T-47D.

Chien-Wei Tseng, Hsuan-Cheng Huang, Arthur Chun-Chieh Shih, Ya-Ya Chang, Chung-Cheng Hsu, Jen-Yun Chang, Wen-Hsiung Li, Hsueh-Fen Juan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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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 4 institutions in 2 countries.

Chien-Wei TsengDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan.
Hsuan-Cheng HuangInstitute of Biomedical Informatics, Center for Systems and Synthetic Biology, National Yang-Ming University, Taipei 112, Taiwan.
Arthur Chun-Chieh ShihInstitute of Information Science, Research Center for Information Technology Innovation, Academia Sinica, Taipei 115, Taiwan.
Ya-Ya ChangDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan.
Chung-Cheng HsuDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan.
Jen-Yun ChangDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan.
Wen-Hsiung LiBiodiversity Research Center and Genomics Research Center, Academia Sinica, Taipei 115, Taiwan.
Hsueh-Fen JuanDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan.ORCID 0000-0003-4876-3309
National Taiwan University · TWNational Yang Ming Chiao Tung University · TWResearch Center for Information Technology Innovation, Academia Sinica · TWUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) cause mRNA degradation or translation suppression of their target genes. Previous studies have found direct involvement of miRNAs in cancer initiation and progression. Artificial miRNAs, designed to target single or multiple genes of interest, provide a new therapeutic strategy for cancer. This study investigates the anti-tumor effect of a novel artificial miRNA, miR P-27-5p, on breast cancer. In this study, we reveal that miR P-27-5p downregulates the differential gene expressions associated with the protein modification process and regulation of cell cycle in T-47D cells. Introduction of this novel artificial miRNA, miR P-27-5p, into breast cell lines inhibits cell proliferation and induces the first "gap" phase (G1) cell cycle arrest in cancer cell lines but does not affect normal breast cells. We further show that miR P-27-5p targets the 3'-untranslated mRNA region (3'-UTR) of cyclin-dependent kinase 4 (CDK4) and reduces both the mRNA and protein level of CDK4, which in turn, interferes with phosphorylation of the retinoblastoma protein (RB1). Overall, our data suggest that the effects of miR p-27-5p on cell proliferation and G1 cell cycle arrest are through the downregulation of CDK4 and the suppression of RB1 phosphorylation. This study opens avenues for future therapies targeting breast cancer.

Indexed as

3' Untranslated RegionsBreast NeoplasmsCell Line, TumorCell ProliferationCyclin-Dependent Kinase 4Down-RegulationFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsPhosphorylationRetinoblastoma Protein3' Untranslated RegionsCDK4 protein, humanCyclin-Dependent Kinase 4MicroRNAsRetinoblastoma Proteinbreast cancercell cyclecyclin-dependent kinase 4exon arraymiR P-27-5pretinoblastoma protein

Identifiers

PMID22754369
PMCPMC3382822
OpenAlexW2068125296

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.