@article {516,
	title = {Autocrine laminin-5 ligates alpha6beta4 integrin and activates RAC and NFkappaB to mediate anchorage-independent survival of mammary tumors.},
	journal = {J Cell Biol},
	volume = {163},
	year = {2003},
	month = {2003 Dec 22},
	pages = {1397-407},
	abstract = {<p>Invasive carcinomas survive and evade apoptosis despite the absence of an exogenous basement membrane. How epithelial tumors acquire anchorage independence for survival remains poorly defined. Epithelial tumors often secrete abundant amounts of the extracellular matrix protein laminin 5 (LM-5) and frequently express alpha6beta4 integrin. Here, we show that autocrine LM-5 mediates anchorage-independent survival in breast tumors through ligation of a wild-type, but not a cytoplasmic tail-truncated alpha6beta4 integrin. alpha6beta4 integrin does not mediate tumor survival through activation of ERK or AKT. Instead, the cytoplasmic tail of beta4 integrin is necessary for basal and epidermal growth factor-induced RAC activity, and RAC mediates tumor survival. Indeed, a constitutively active RAC sustains the viability of mammary tumors lacking functional beta1 and beta4 integrin through activation of NFkappaB, and overexpression of NFkappaB p65 mediates anchorage-independent survival of nonmalignant mammary epithelial cells. Therefore, epithelial tumors could survive in the absence of exogenous basement membrane through autocrine LM-5-alpha6beta4 integrin-RAC-NFkappaB signaling.</p>
},
	keywords = {Autocrine Communication, Basement Membrane, Breast Neoplasms, Carcinoma, Cell Adhesion, Cell Adhesion Molecules, Cell Line, Tumor, Cell Survival, Epidermal Growth Factor, Humans, Integrin alpha6beta4, MAP Kinase Signaling System, Neoplasm Invasiveness, NF-kappa B, Protein Structure, Tertiary, rac GTP-Binding Proteins},
	issn = {0021-9525},
	doi = {10.1083/jcb.200302023},
	author = {Zahir, Nastaran and Lakins, Johnathon N and Russell, Alan and Ming, WenYu and Chatterjee, Chandrima and Rozenberg, Gabriela I and Marinkovich, M Peter and Weaver, Valerie M}
}
@article {541,
	title = {Tumour-stromal interactions. Integrins and cell adhesions as modulators of mammary cell survival and transformation.},
	journal = {Breast Cancer Res},
	volume = {3},
	year = {2001},
	month = {2001},
	pages = {224-9},
	abstract = {<p>Stromal-epithelial interactions modulate mammary epithelial cell (MEC) growth and apoptosis by influencing cell adhesion and tissue organization. Perturbations in the mammary stroma and cell adhesion characterize breast tumors and underlie the altered tissue organization, disrupted tissue homeostasis and enhanced survival phenotype of the disease. Apoptosis resistance likely arises during malignant transformation via genetic and epigenetic modification of cell adhesion pathways induced by a changing tissue microenvironment. Acquisition of adhesion-linked survival networks that enhance MEC viability in the absence of basement membrane interactions probably promote malignant transformation, and may render breast tumors sufficiently resistant to exogenous apoptotic stimuli to generate multidrug resistance.</p>
},
	keywords = {Apoptosis, Basement Membrane, Breast Neoplasms, Cell Adhesion Molecules, Cell Communication, Cell Differentiation, Cell Survival, Cell Transformation, Neoplastic, Drug Resistance, Multiple, Epithelial Cells, Female, Gene Expression Regulation, Neoplastic, Humans, Integrins, Stromal Cells},
	issn = {1465-5411},
	author = {Chrenek, M A and Wong, P and Weaver, V M}
}
