@article {766,
	title = {Tumor-induced solid stress activates β-catenin signaling to drive malignant behavior in normal, tumor-adjacent cells.},
	journal = {Bioessays},
	volume = {37},
	year = {2015},
	month = {2015 Dec},
	pages = {1293-7},
	abstract = {<p>Recent work by Fern{\'a}ndez-S{\'a}nchez and coworkers examining the impact of applied pressure on the malignant phenotype of murine colon tissue in vivo revealed that mechanical perturbations can drive malignant behavior in genetically normal cells. Their findings build upon an existing understanding of how the mechanical cues experienced by cells within a tissue become progressively modified as the tissue transforms. Using magnetically stimulated ultra-magnetic liposomes to mimic tumor growth -induced solid stress, Fern{\'a}ndez-S{\'a}nchez and coworkers were able to stimulate β-catenin to promote the cancerous behavior of both a normal and genetically modified colon epithelium. In this perspective, we discuss their findings in the context of what is currently known regarding the role of the mechanical landscape in cancer progression and β-catenin as a mechanotransducer. We review data that suggest that mechanically regulated activation of β-catenin fosters development of a malignant phenotype in tissue and predict that mechanical cues may contribute to tumor heterogeneity.</p>
},
	issn = {1521-1878},
	doi = {10.1002/bies.201500090},
	author = {Ou, Guanqing and Weaver, Valerie Marie}
}
@article {226,
	title = {Tissue mechanics modulate microRNA-dependent PTEN expression to regulate malignant progression.},
	journal = {Nat Med},
	year = {2014},
	month = {2014 Mar 16},
	abstract = {<p>Tissue mechanics regulate development and homeostasis and are consistently modified in tumor progression. Nevertheless, the fundamental molecular mechanisms through which altered mechanics regulate tissue behavior and the clinical relevance of these changes remain unclear. We demonstrate that increased matrix stiffness modulates microRNA expression to drive tumor progression through integrin activation of β-catenin and MYC. Specifically, in human and mouse tissue, increased matrix stiffness induced miR-18a to reduce levels of the tumor suppressor phosphatase and tensin homolog (PTEN), both directly and indirectly by decreasing levels of homeobox A9 (HOXA9). Clinically, extracellular matrix stiffness correlated directly and significantly with miR-18a expression in human breast tumor biopsies. miR-18a expression was highest in basal-like breast cancers in which PTEN and HOXA9 levels were lowest, and high miR-18a expression predicted poor prognosis in patients with luminal breast cancers. Our findings identify a mechanically regulated microRNA circuit that can promote malignancy and suggest potential prognostic roles for HOXA9 and miR-18a levels in stratifying patients with luminal breast cancers.</p>
},
	issn = {1546-170X},
	doi = {10.1038/nm.3497},
	author = {Mouw, Janna K and Yui, Yoshihiro and Damiano, Laura and Bainer, Russell O and Lakins, Johnathon N and Acerbi, Irene and Ou, Guanqing and Wijekoon, Amanda C and Levental, Kandice R and Gilbert, Penney M and Hwang, E Shelley and Chen, Yunn-Yi and Weaver, Valerie M}
}
