AIM: To detect the mechanism by which @entity694 escapes the growth constraints imposed on normal cells by cell crowding and dense pericellular matrices. METHODS: An immunohistochemical study of integrin avb6 and @entity1495 ( @entity1495 ) was performed on tissue microarrays of 200 spots, including 100 cases of @entity694 . RESULTS: High immunoreactivity for avb6 (73.7%; 28/38) and @entity1495 (76.5%; 52/68) was observed in invasive @entity5 portions. Furthermore, the effects of integrin avb6 on @entity5 @entity851 in @entity19 were detected. Tumor @entity851 and high expression of both avb6 and @entity1495 were only seen in @entity5 resulting from WiDr cells expressing avb6 in the tumorigenicity assay. Flow cytometry was applied to analyze avb6 expression in @entity694 WiDr and SW480 cells. The effects of cell density on avb6 expression and @entity1495 secretion were also detected by Biotrak @entity1495 activity assay and gelatin zymography assay. High cell density evidently enhanced avb6 expression and promoted @entity1495 secretion compared with low density. CONCLUSION: Integrin avb6 sustains and promotes @entity5 @entity851 in @entity5 progression via a self-perpetuating mechanism. Integrin a  b6-mediated @entity1495 secretion facilitates pericellular matrix degradation at high cell density, which provides the basis of @entity851 .

Integrin avb6 sustains and promotes @entity5 XXXX in @entity694 progression.

@entity851 :: ('MESH:D006130', 'Disease') :: ['invasive growth'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'tumors'] @entity19 :: ('10090', 'Species') :: ['nude mice'] @entity1495 :: ('4318', 'Gene') :: ['MMP-9', 'matrix metalloproteinase-9'] @entity694 :: ('MESH:D003110', 'Disease') :: ['colon tumors', 'colon tumor', 'colon cancer']
@entity851 :: (MESH:D006130,Disease) :: ['invasive growth']
