@article {256,
	title = {Oncogenic targeting of BRM drives malignancy through C/EBPβ-dependent induction of α5 integrin.},
	journal = {Oncogene},
	year = {2013},
	month = {2013 Jun 17},
	abstract = {<p>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.Oncogene advance online publication, 17 June 2013; doi:10.1038/onc.2013.220.</p>
},
	issn = {1476-5594},
	doi = {10.1038/onc.2013.220},
	author = {Damiano, L and Stewart, K M and Cohet, N and Mouw, J K and Lakins, J N and Debnath, J and Reisman, D and Nickerson, J A and Imbalzano, A N and Weaver, V M}
}
@article {396,
	title = {Biomechanical regulation of cell orientation and fate.},
	journal = {Oncogene},
	volume = {27},
	year = {2008},
	month = {2008 Nov 24},
	pages = {6981-93},
	abstract = {<p>Biomechanical regulation of tumor phenotypes have been noted for several decades, yet the function of mechanics in the co-evolution of the tumor epithelium and altered cancer extracellular matrix has not been appreciated until fairly recently. In this review, we examine the dynamic interaction between the developing epithelia and the extracellular matrix, and discuss how similar interactions are exploited by the genetically modified epithelium during tumor progression. We emphasize the process of mechanoreciprocity, which is a phenomenon observed during epithelial transformation, in which tension generated within the extracellular microenvironment induce and cooperate with opposing reactive forces within transformed epithelium to drive tumor progression and metastasis. We highlight the importance of matrix remodeling, and present a new, emerging paradigm that underscores the importance of tissue morphology as a key regulator of epithelial cell invasion and metastasis.</p>
},
	keywords = {Animals, Biochemical Processes, Bioreactors, Cell Culture Techniques, Cell Differentiation, Cell Movement, Cell Polarity, Cell Transformation, Neoplastic, Embryonic Development, Epithelial Cells, Humans, Mechanotransduction, Cellular, Models, Biological, Neoplasm Metastasis},
	issn = {1476-5594},
	doi = {10.1038/onc.2008.348},
	author = {Lopez, J I and Mouw, J K and Weaver, V M}
}
