Evidence map›Paper›PMID 25266720›Full record

ArticleThe Journal of biological chemistry2014

MicroRNA-125a reduces proliferation and invasion of oral squamous cell carcinoma cells by targeting estrogen-related receptor α: implications for cancer therapeutics.

Ankana Tiwari, Swamy Shivananda, Kodaganur S Gopinath, Arun Kumar

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  15. MiRNA373 induces cervical squamous cell carcinoma SiHa cell apoptosis.Cancer biomarkers : section A of Disease markers · 2018
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  19. Review
  20. ERRα Is a Marker of Tamoxifen Response and Survival in Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ankana TiwariDepartment of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore 560012 and.
Swamy ShivanandaDepartment of Surgery, Bangalore Institute of Oncology, Bangalore 560027, India.
Kodaganur S GopinathDepartment of Surgery, Bangalore Institute of Oncology, Bangalore 560027, India.
Arun KumarDepartment of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore 560012 and. Electronic address: karun@mrdg.iisc.ernet.in.
Indian Institute of Science Bangalore · INKidwai Memorial Institute of Oncology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen-related receptor α (ESRRA) functions as a transcription factor and regulates the expression of several genes, such as WNT11 and OPN. Up-regulation of ESRRA has been reported in several cancers. However, the mechanism underlying its up-regulation is unclear. Furthermore, the reports regarding the role and regulation of ESRRA in oral squamous cell carcinoma (OSCC) are completely lacking. Here, we show that tumor suppressor miR-125a directly binds to the 3'UTR of ESRRA and represses its expression. Overexpression of miR-125a in OSCC cells drastically reduced the level of ESRRA, decreased cell proliferation, and increased apoptosis. Conversely, the delivery of an miR-125a inhibitor to these cells drastically increased the level of ESRRA, increased cell proliferation, and decreased apoptosis. miR-125a-mediated down-regulation of ESRRA impaired anchorage-independent colony formation and invasion of OSCC cells. Reduced cell proliferation and increased apoptosis of OSCC cells were dependent on the presence of the 3'UTR in ESRRA. The delivery of an miR-125a mimic to OSCC cells resulted in marked regression of xenografts in nude mice, whereas the delivery of an miR-125a inhibitor to OSCC cells resulted in a significant increase of xenografts and abrogated the tumor suppressor function of miR-125a. We observed an inverse correlation between the expression levels of miR-125a and ESRRA in OSCC samples. In summary, up-regulation of ESRRA due to down-regulation of miR-125a is not only a novel mechanism for its up-regulation in OSCC, but decreasing the level of ESRRA by using a synthetic miR-125a mimic may have an important role in therapeutic intervention of OSCC and other cancers.

Indexed as

Gene Expression Regulation, NeoplasticAmino Acid SequenceAnimalsApoptosisAzacitidineCarcinoma, Squamous CellCell Line, TumorCell ProliferationDecitabineEstrogen Receptor alphaFemaleHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsAzacitidineDecitabineESR1 protein, humanEstrogen Receptor alphaMicroRNAsMIRN125 microRNA, humanCancer BiologyCell ProliferationHead and Neck Squamous Cell CarcinomaMicroRNA (miRNA)Post-transcriptional Regulation

Identifiers

PMID25266720
PMCPMC4231701
OpenAlexW2060080575

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.