Intercellular adhesions share the complex task of establishing and maintaining tissue architecture while allowing tissue growth, renewal and repair.
ALCAM is localized at intercellular junctions in epithelium presumably as part of the adhesive complex that maintains tissue architecture.
In epithelial tissues, several classes of proteins are involved in maintaining tissue architecture, including those that promote cell cell adhesion, and others, which mediate cell matrix interactions.
These data demonstrate that primary human prostate xenografts, benign and malignant, can be established routinely from human prostate tissue surgical specimens, and that the xenografts maintain tissue architecture and expression of key prostatic markers.
In the central nervous system, the junctional types that establish and maintain tissue architecture include gap junctions, for cytoplasmic connectivity, and tight junctions, for paracellular and/or cell polarity barriers.
These results confirm the role of these proteins in maintaining tissue architecture and in inhibiting cell invasiveness and potentially indicate the oncogenic potential of the Wnt/β-catenin transduction pathway in feline mammary tumours.
The regulation of epithelial cell-cell adhesion is of utmost importance to maintain tissue architecture and to prevent cell invasion during pathological conditions [19], [54], and E-cadherin is a primordial factor often repressed during transition from adenoma to carcinoma [20], [55].
Critical to maintain tissue architecture is the extracellular matrix, a major component of the cellular microenvironment.
The microenvironment provides crucial signaling to maintain tissue architecture, inhibit cell growth, and modulate differentiated phenotypes.
Integrins maintain tissue architecture and function in the normal breast, while disrupting the integrin axis alters signalling and causes tissue disorganisation and malignancy.
