The tension mounts: mechanics meets morphogenesis and malignancy.

TitleThe tension mounts: mechanics meets morphogenesis and malignancy.
Publication TypeJournal Article
Year of Publication2004
AuthorsPaszek MJ, Weaver VM
JournalJ Mammary Gland Biol Neoplasia
Volume9
Issue4
Pagination325-42
Date Published2004 Oct
ISSN1083-3021
KeywordsAnimals, Biomechanical Phenomena, Cell Transformation, Neoplastic, Homeostasis, Humans, Morphogenesis, Neoplasms
Abstract

The tissue microenvironment regulates mammary gland development and tissue homeostasis through soluble, insoluble and cellular cues that operate within the three dimensional architecture of the gland. Disruption of these critical cues and loss of tissue architecture characterize breast tumors. The developing and lactating mammary gland are also subject to a plethora of tensional forces that shape the morphology of the gland and orchestrate its functionally differentiated state. Moreover, malignant transformation of the breast is associated with dramatic changes in gland tension that include elevated compression forces, high tensional resistance stresses and increased extracellular matrix stiffness. Chronically increased mammary gland tension may influence tumor growth, perturb tissue morphogenesis, facilitate tumor invasion, and alter tumor survival and treatment responsiveness. Because mammary tissue differentiation is compromised by high mechanical force and transformed cells exhibit altered mechanoresponsiveness, malignant transformation of the breast may be functionally linked to perturbed tensional-homeostasis. Accordingly, it will be important to define the role of tensional force in mammary gland development and tumorigenesis. Additionally, it will be critical to identify the key molecular elements regulating tensional-homeostasis of the mammary gland and thereafter to characterize their associated mechanotransduction pathways.

DOI10.1007/s10911-004-1404-x
Alternate JournalJ Mammary Gland Biol Neoplasia
PubMed ID15838603
Grant ListCA078731 / CA / NCI NIH HHS / United States
HL6438801A1 / HL / NHLBI NIH HHS / United States