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RKIp inhibits the migration and invasion of human prostate cancer PC-3M cells through regulation of extracellular matrix.


Raf kinase inhibitor protein (RKIP) plays a pivotal role in several intracellular signaling cascades and has been implicated as a metastasis suppressor in multiple cancer cells including prostate cancer cells, but the mechanism is not very clear. In this study, we investigated the effect of RKIP on cell proliferation, migration and invasion using human prostate cancer PC-3M cells as a model system. Our results indicate that RKIP does not effect cell proliferation in PC-3M cells, but inhibits both cell migration and cell invasion. In association with this inhibitory effect, RKIP down-regulates matrix metalloproteinases (MMP-2 and MMP-9), cathepsin B and urinary plasminogen activator (uPA). Also RKIP has the ability to regulate the expression of E-cadherin. But ectopic expression of RKIP does not affect the level of the Snail protein. As it has been indicated here, RKIP inhibits the migration and invasion ability of human prostate cancer cells through regulation of the extracellular matrix. These findings provide new mechanistic insight how RKIP suppresses metastasis in vitro.

Authors+Show Affiliations


Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, College of Life Sciences, Beijing Normal University, 100875.

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Molekuliarnaia biologiia 45:6 pg 1004-11


Cathepsin B
Cell Line, Tumor
Cell Movement
Cell Proliferation
Extracellular Matrix
Gene Expression Regulation, Neoplastic
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Neoplasm Invasiveness
Phosphatidylethanolamine Binding Protein
Prostatic Neoplasms
Urokinase-Type Plasminogen Activator

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't



PubMed ID