Evidence map›Paper›PMID 27100732›Full record

ArticleBritish journal of cancer2016

Regulation of the T-box transcription factor Tbx3 by the tumour suppressor microRNA-206 in breast cancer.

Sumaira Amir, Catalina Simion, Maxine Umeh-Garcia, Sheryl Krig, Tyler Moss, Kermit L Carraway, Colleen Sweeney

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
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  4. Wnt Signaling and Aging of the Gastrointestinal Tract.International journal of molecular sciences · 2022
    Review
  5. Article
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  9. Review
  10. The potential oncogenic role of the RAS-like GTP-binding gene RIT1 in glioblastoma.Cancer biomarkers : section A of Disease markers · 2020
    Article
  11. Article
  12. Article
  13. Expression of TBX3 in Hepatocellular Carcinoma and Its Clinical Implication.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  14. The oncomir face of microRNA-206: A permanent miR-206 transfection study.Experimental biology and medicine (Maywood, N.J.) · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. MicroRNA in breast cancer: The association with BRCA1/2.Cancer biomarkers : section A of Disease markers · 2017
    Review
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 2 institutions in 1 country.

Sumaira AmirDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Catalina SimionDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Maxine Umeh-GarciaDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Sheryl KrigDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Tyler MossDepartment of Systems Biology, MD Anderson Cancer Center, Houston, TX 77054, USA.
Kermit L CarrawayDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Colleen SweeneyDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
University of California, Davis · USThe University of Texas MD Anderson Cancer Center · US

Funding

UC Davis MCB T32 Administrative Supplement to Recognize Excellence in Diversity, Equity, Inclusion, and Accessibility (DEIA) MentorshipT32GM007377 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI CHEDIN, FREDERIC LOUIS · 1985 to 2023
$9.9M
Muc4 Involvement in Mammary Tumor ProgressionR01CA166412 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2013 to 2017
$1.5M
NCI NIH HHS R01 CA166412NIGMS NIH HHS T32 GM007377
6 · The paper itself

Abstract

backgroundThe Tbx3 transcription factor is over-expressed in breast cancer, where it has been implicated in proliferation, migration and regulation of the cancer stem cell population. The mechanisms that regulate Tbx3 expression in cancer have not been fully explored. In this study, we demonstrate that Tbx3 is repressed by the tumour suppressor miR-206 in breast cancer cells.

methodsBioinformatics prediction programmes and luciferase reporter assays were used to demonstrate that miR-206 negatively regulates Tbx3. We examined the impact of miR-206 on Tbx3 expression in breast cancer cells using miR-206 mimic and inhibitor. Gene/protein expression was examined by quantitative reverse-transcription-PCR and immunoblotting. The effects of miR-206 and Tbx3 on apoptosis, proliferation, invasion and cancer stem cell population was investigated by cell-death detection, colony formation, 3D-Matrigel and tumorsphere assays.

resultsIn this study, we examined the regulation of Tbx3 by miR-206. We demonstrate that Tbx3 is directly repressed by miR-206, and that this repression of Tbx3 is necessary for miR-206 to inhibit breast tumour cell proliferation and invasion, and decrease the cancer stem cell population. Moreover, Tbx3 and miR-206 expression are inversely correlated in human breast cancer. Kaplan-Meier analysis indicates that patients exhibiting a combination of high Tbx3 and low miR-206 expression have a lower probability of survival when compared with patients with low Tbx3 and high miR-206 expression. These studies uncover a novel mechanism of Tbx3 regulation and identify a new target of the tumour suppressor miR-206.

conclusionsThe present study identified Tbx3 as a novel target of tumour suppressor miR-206 and characterised the miR-206/Tbx3 signalling pathway, which is involved in proliferation, invasion and maintenance of the cancer stem cell population in breast cancer cells. Our results suggest that restoration of miR-206 in Tbx3-positive breast cancer could be exploited for therapeutic benefit.

Indexed as

ApoptosisBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationComputational BiologyFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsPrognosisSurvival AnalysisT-Box Domain ProteinsMicroRNAsMIRN206 microRNA, humanT-Box Domain ProteinsTBX3 protein, human

Identifiers

PMID27100732
PMCPMC4865973
OpenAlexW2338653279

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.