ArticleOncogene2014
Oncogenic targeting of BRM drives malignancy through C/EBPβ-dependent induction of α5 integrin.
Article in Oncogene, 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 It has been retracted, and should not be counted.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 10 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- High expression of SMARCA4 or SMARCA2 is frequently associated with an opposite prognosis in cancer.Scientific reports · 2018Pooled it
- BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- A Swedish Familial Genome-Wide Haplotype Analysis Identified Five Novel Breast Cancer Susceptibility Loci on 9p24.3, 11q22.3, 15q11.2, 16q24.1 and Xq21.31.International journal of molecular sciences · 2023Article
- α5β1-Integrin promotes tension-dependent mammary epithelial cell invasion by engaging the fibronectin synergy site.Molecular biology of the cell · 2017Article
- Hypoxia Selectively Enhances Integrin αMolecular cancer research : MCR · 2017Article
- Identification of Novel Regulators of the JAK/STAT Signaling Pathway that Control Border Cell Migration in the Drosophila Ovary.G3 (Bethesda, Md.) · 2016Article
- Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression.Nature medicine · 2016Article
- The SWI/SNF ATPases Are Required for Triple Negative Breast Cancer Cell Proliferation.Journal of cellular physiology · 2015Article
- Dense fibrillar collagen is a potent inducer of invadopodia via a specific signaling network.The Journal of cell biology · 2015Article
- Modulation of Brahma expression by the mitogen-activated protein kinase/extracellular signal regulated kinase pathway is associated with changes in melanoma proliferation.Archives of biochemistry and biophysics · 2014Article
Corrections and comments
- Retraction · 2024-02-23Duplication of/in Image · Error in Image ·
- Retracted
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Integrin expression and activity are altered in tumors, and aberrant integrin signaling promotes malignancy. However, how integrins become altered in tumors remains poorly understood. We discovered that oncogenic activation of MEK signaling induces cell growth and survival, and promotes the malignant phenotype of mammary epithelial cells (MECs) by increasing α5 integrin expression. We determined that MEK activates c-Myc to reduce the transcription of the SWI/SNF chromatin remodeling enzyme Brahma (BRM). Our studies revealed that reduced BRM expression and/or activity drives the malignant behavior of MECs by epigenetically promoting C/EBPβ expression to directly induce α5 integrin transcription. Consistently, we could show that restoring BRM levels normalized the malignant behavior of transformed MECs in culture and in vivo by preventing C/EBPβ-dependent α5 integrin transcription. Our findings identify a novel mechanism whereby oncogenic signaling promotes malignant transformation by regulating transcription of a key chromatin remodeling molecule that regulates integrin-dependent stromal-epithelial interactions.
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Registered trials
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.