New therapies for late stage and castration resistant prostate cancer CRPC depend on defining unique properties and pathways of cell sub-populations capable of sustaining the net growth of the cancer. We have shown previously that the LSC hi subpopulation is both necessary and sufficient for cancer initiation in the Pten -null prostate cancer model.
To further improve this enrichment scheme, we searched for cell surface molecules upregulated upon castration of murine prostate and identified CD as a candidate gene. Importantly, CD could enrich sphere-forming ability of benign primary human prostate cells in vitro and induce the formation of tubule-like structures in vivo. Editor: Dean G. Tang, The University of Texas M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist.
Despite advances in the early detection and management of prostate cancer, castration resistant prostate cancer CRPC remains the second most common cause of male mortality in the United States [1]. Mounting evidence suggests that a subpopulation of prostate cells can initiate prostate cancer and may be responsible for the castration resistance [2] , [3] , [4] , [5].
Therefore, these cancer initiating cells [6] may serve as promising cellular targets for prostate cancer and identification of this subpopulation has become the necessary step toward future effective therapy.
