@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 {526,
	title = {The organizing principle: microenvironmental influences in the normal and malignant breast.},
	journal = {Differentiation},
	volume = {70},
	year = {2002},
	month = {2002 Dec},
	pages = {537-46},
	abstract = {<p>The current paradigm for cancer initiation and progression rests on the groundbreaking discoveries of oncogenes and tumor suppressor genes. This framework has revealed much about the role of genetic alterations in the underlying signaling pathways central to normal cellular function and to tumor progression. However, it is clear that single gene theories or even sequential acquisition of mutations underestimate the nature of the genetic and epigenetic changes in tumors, and do not account for the observation that many cancer susceptibility genes (e.g. BRCA1, APC) show a high degree of tissue specificity in their association with neoplastic transformation. Therefore, the cellular and tissue context itself must confer additional and crucial information necessary for mutated genes to exert their influence. A considerable body of evidence now shows that cell-cell and cell-extracellular matrix (ECM) interactions are essential organizing principles that help define the nature of the tissue context, and play a crucial role in regulating homeostasis and tissue specificity. How this context determines functional integrity, and how its loss can lead to malignancy, appears to have much to do with tissue structure and polarity.</p>
},
	keywords = {Apoptosis, Breast, Breast Neoplasms, Coculture Techniques, Female, Humans, Signal Transduction},
	issn = {0301-4681},
	doi = {10.1046/j.1432-0436.2002.700907.x},
	author = {Bissell, Mina J and Radisky, Derek C and Rizki, Aylin and Weaver, Valerie M and Petersen, Ole W}
}
