Evidence map›Paper›PMID 20659323›Full record

ArticleBreast cancer research : BCR2010

MYB suppresses differentiation and apoptosis of human breast cancer cells.

Yvette Drabsch, Ramsay G Robert, Thomas J Gonda

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  4. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
  5. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
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  19. Overexpression of c-Myb is associated with suppression of distant metastases in colorectal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Yvette DrabschUniversity of Queensland Diamantina Institute, University of Queensland, Ipswich Road, Brisbane, Queensland, 4102, Australia.
Ramsay G Robert
Thomas J Gonda
University of Queensland · AUPeter MacCallum Cancer Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMYB is highly expressed in estrogen receptor positive (ER + ve) breast tumours and tumour cell lines. We recently demonstrated that MYB is essential for the proliferation of ER + ve breast cancer cells, and have now investigated its role in mammary epithelial differentiation.

methodsMCF-7 breast cancer cells were treated with sodium butyrate, vitamin E succinate or 12-O-tetradecanoylphorbol-13-acetate to induce differentiation as measured by Nile Red staining of lipid droplets and β-casein expression. The non-tumorigenic murine mammary epithelial cell (MEC) line, HC11, was induced to differentiate with lactogenic hormones. MYB levels were manipulated by inducible lentiviral shRNA-mediated knockdown and retroviral overexpression.

resultsWe found that MYB expression decreases following chemically-induced differentiation of the human breast cancer cell line MCF-7, and hormonally-induced differentiation of a non-tumorigenic murine mammary epithelial cell (MEC) line, HC11. We also found that shRNA-mediated MYB knockdown initiated differentiation of breast cancer cells, and greatly sensitised them to the differentiative and pro-apoptotic effects of differentiation-inducing agents (DIAs). Sensitisation to the pro-apoptotic effects DIAs is mediated by decreased expression of BCL2, which we show here is a direct MYB target in breast cancer cells. Conversely, enforced expression of MYB resulted in the cells remaining in an undifferentiated state, with concomitant suppression of apoptosis, in the presence of DIAs.

conclusionsTaken together, these data imply that MYB function is critical in regulating the balance between proliferation, differentiation, and apoptosis in MECs. Moreover, our findings suggest MYB may be a viable therapeutic target in breast cancer and suggest specific approaches for exploiting this possibility.

Indexed as

AnimalsApoptosisBlotting, WesternBreast NeoplasmsButyratesCell DifferentiationCell LineCell Line, TumorDrug SynergismEstradiolEstrogen AntagonistsFemaleFulvestrantGene ExpressionGreen Fluorescent ProteinsHumansButyratesEstradiolEstrogen AntagonistsFulvestrantGreen Fluorescent ProteinsProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mybTetradecanoylphorbol AcetateVitamin EVitamins

Identifiers

PMID20659323
PMCPMC2949644
OpenAlexW2109287818

What OpenQuestion holds

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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.