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Previous reports demonstrate that the  α 2-integrin ( α 2) mediates pancreatic ductal adenocarcinoma (PDAC) cell interactions with collagens. We found that while well-differentiated cells use  α 2 exclusively to adhere and migrate on collagenI, poorly differentiated PDAC cells demonstrate reduced reliance on, or complete loss of,  α 2. Since well-differentiated PDAC lines exhibit reduced  in vitro  invasion and  α 2-blockade suppressed invasion of well-differentiated lines exclusively, we hypothesized that  α 2 may suppress the malignant phenotype in PDAC. Accordingly, ectopic expression of  α 2 retarded  in vitro  invasion and maintenance on collagenI exacerbated this effect. Affymetrix profiling revealed that kallikrein-related peptidase-5 (KLK5) was specifically upregulated by  α 2, and reduced  α 2 and KLK5 expression was observed in poorly differentiated PDAC cells  in situ . Accordingly, well-differentiated PDAC lines express KLK5, and KLK5 blockade increased the invasion of KLK5-positive lines. The  α 2-cytoplasmic domain was dispensable for these effects, demonstrating that the  α 2-ectodomain and KLK5 coordinately regulate a less invasive phenotype in PDAC.

α2 Integrin-Dependent Suppression of Pancreatic Adenocarcinoma Cell Invasion Involves Ectodomain Regulation of Kallikrein-Related Peptidase-5