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Cancer metastasis database
General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction

Basic Information

Gene ID

5300

Name

PIN1

Synonymous

peptidylprolyl cis/trans isomerase, NIMA-interacting 1;PIN1;peptidylprolyl cis/trans isomerase, NIMA-interacting 1

Definition

PPIase Pin1|peptidyl-prolyl cis-trans isomerase NIMA-interacting 1|protein (peptidyl-prolyl cis/trans isomerase) NIMA-interacting 1|rotamase Pin1

Position

19p13

Gene type

protein-coding

Title

Abstract

breast cancer

Pin-1 has been shown to regulate several phases of the cell cycle and is strikingly overexpressed in many human cancers. Vascular endothelial growth factor (VEGF)-C is a potent lymphangiogenic factor produced by tumor and stromal cells. However, little is known about the roles of Pin-1 and VEGF-C in breast carcinoma. p53 protein and cyclin D1 overexpressions have been shown to play a role as prognostic factors in many human cancers. To better understand the roles of Pin-1 and VEGF-C in breast carcinoma, we evaluated the immunohistochemical expression of Pin-1 and VEGF-C in relationship with p53 protein or cyclin D1 overexpression and clinicopathological parameters in 128 mammary infiltrating duct carcinomas. There was a positive expression in 100% of Pin-1, 88% of VEGF-C, 35% of p53 protein, and 66% of cyclin D1 in the breast carcinoma. Correlation of the positive expression of Pin-1 with tumor grade (p<0.01) and lymph node metastasis or cyclin D1 overexpression (p<0.05, respectively) was statistically significant. Significant correlation was observed between VEGF-C and tumor grade, lymph node metastasis or clinical stage (p<0.01, respectively). These results indicate that elevated Pin-1 or VEGF-C expression is more common in infiltrating duct carcinomas with poor prognostic characteristics and is partly associated with an unfavorable outcome. Given the role of cyclin D1 overexpression in oncogenesis of breast, these results suggest that overexpression of Pin-1 and VEGF-C may promote tumor progression and metastasis.