Gene expression profiling of human prostate cancer stem cells reveals a pro-inflammatory phenotype and the importance of extracellular matrix interactions

Richard Birnie,Alastair Droop,Paul A Berry,Anne T Collins,Vincent Dussupt,Catherine F Hyde,Norman J Maitland,John L Lewis,Steven D Bryce,Shona H Lang,Claire Roome,Michael J Stower

doi:10.1186/gb-2008-9-5-r83

Abstract

An expression signature of human prostate cancer stem cells identifies 581 differentially expressed genes and suggests that the JAK-STAT pathway and focal adhesion signaling are important.

Highlights

The tumor-initiating capacity of many cancers is considered to reside in a small subpopulation of cells
We have recently shown that a rare cell population in human prostate cancer, defined by the phenotype CD133+/α2β1hi and comprising less than 0.1% of the tumor mass, has many of the properties of cancer stem cells [4]
Within the different disease states we found that samples with the same differentiation state clustered together (Figure 1a)

Summary

Introduction

The tumor-initiating capacity of many cancers is considered to reside in a small subpopulation of cells (cancer stem cells). We have previously shown that rare prostate epithelial cells with a CD133+/α2β1hi phenotype have the properties of prostate cancer stem cells. In leukaemia, the ability to initiate new tumor growth resides in a rare phenotypically distinct subset of tumor cells [3] that are defined by the expression of CD34+CD38- surface antigens and have been termed leukemic stem cells. We have recently shown that a rare cell population in human prostate cancer, defined by the phenotype CD133+/α2β1hi (high expression of α2β1 integrin) and comprising less than 0.1% of the tumor mass, has many of the properties of cancer stem cells [4]. Self renewal, extended lifespan (compared to normal stem cells), a high invasive capacity, a primitive epithelial phenotype and an ability to differentiate to recapitulate the phenotypes seen in prostate tumors. The cancer stem cell content was not, dependent on prostate tumor clinical stage or grade

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Discussion

Conclusion