ArticleStem cells (Dayton, Ohio)2014
YB-1 transforms human mammary epithelial cells through chromatin remodeling leading to the development of basal-like breast cancer.
Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Epigenetic and O-glycosylation regulation of p66Shc mitigates mitochondrial oxidative stress in aortic dissection.Theranostics · 2026Article
- Oncolytic virotherapy provides a potent therapy option for squamous bladder cancer.Scientific reports · 2025Article
- Y-box binding protein 1/cyclin A1 axis specifically promotes cell cycle progression at GScientific reports · 2024Article
- KMT2D-mediated H3K4me1 recruits YBX1 to facilitate triple-negative breast cancer progression through epigenetic activation of c-Myc.Clinical and translational medicine · 2024Article
- YB1 modulates the DNA damage response in medulloblastoma.Scientific reports · 2023Article
- The CDK4/6 Inhibitor Palbociclib Inhibits Estrogen-Positive and Triple Negative Breast Cancer Bone Metastasis In Vivo.Cancers · 2023Article
- The dual distinct role of telomerase in repression of senescence and myofibroblast differentiation.Aging · 2021Article
- Association BetweenFrontiers in genetics · 2021Review
- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
- A Novel Ten-Gene Signature Predicting Prognosis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020Article
- Article
- Oncogenic Y-box binding protein-1 as an effective therapeutic target in drug-resistant cancer.Cancer science · 2019Review
- Single-cell landscape in mammary epithelium reveals bipotent-like cells associated with breast cancer risk and outcome.Communications biology · 2019Article
- Y-box binding protein YBX1 and its correlated genes as biomarkers for poor outcomes in patients with breast cancer.Oncotarget · 2018Article
- Crosstalk between Akt signaling and cold shock proteins in mediating invasive cell phenotypes.Oncotarget · 2018Article
- ERα Binding by Transcription Factors NFIB and YBX1 Enables FGFR2 Signaling to Modulate Estrogen Responsiveness in Breast Cancer.Cancer research · 2018Article
- Article
- Centrosome amplification: a suspect in breast cancer and racial disparities.Endocrine-related cancer · 2017Review
- A Tox21 Approach to Altered Epigenetic Landscapes: Assessing Epigenetic Toxicity Pathways Leading to Altered Gene Expression and Oncogenic Transformation In Vitro.International journal of molecular sciences · 2017Review
- Aloe-emodin inhibits HER-2 expression through the downregulation of Y-box binding protein-1 in HER-2-overexpressing human breast cancer cells.Oncotarget · 2016Article
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Authors and funding
12 authors.
Funding
Abstract
There is growing evidence that cancer-initiation could result from epigenetic changes. Y-box binding protein-1 (YB-1) is a transcription/translation factor that promotes the formation of tumors in transgenic mice; however, the underlying molecular events are not understood. To explore this in a human model system, YB-1 was expressed in mammary epithelial cells under the control of a tetracycline-inducible promoter. The induction of YB-1 promoted phenotypes associated with malignancy in three-dimensional breast acini cultures. This was attributed to YB-1 enhancing the expression and activity of the histone acetyltransferase p300 leading to chromatin remodeling. Specifically, this relaxation of chromatin allowed YB-1 to bind to the BMI1 promoter. The induction of BMI1 engaged the Polycomb complex resulting in histone H2A ubiquitylation and repression of the CDKN2A locus. These events manifested functionally as enhanced self-renewal capacity that occurred in a BMI1-dependent manner. Conversely, p300 inhibition with anacardic acid prevented YB-1 from binding to the BMI1 promoter and thereby subverted self-renewal. Despite these early changes, full malignant transformation was not achieved until RSK2 became overexpressed concomitant with elevated human telomerase reverse transcriptase (hTERT) activity. The YB-1/RSK2/hTERT expressing cells formed tumors in mice that were molecularly subtyped as basal-like breast cancer. We conclude that YB-1 cooperates with p300 to allow BMI1 to over-ride p16(INK4a) -mediated cell cycle arrest enabling self-renewal and the development of aggressive breast tumors.
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