Journal
ONCOTARGET
Volume 6, Issue 2, Pages 1202-1216Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.2841
Keywords
androgen deprivation therapy; epithelial-mesenchymal transition; TGF beta 1; cancer stem cell; CD44; prostate cancer
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Funding
- National Basic Research Program of China [2012CB518304]
- TSTC grant [2012DFG32220]
- National Natural Science Foundation for Young Scholars of China [81302211, 81202024]
- Ph.D Programs Foundation of Ministry of Education of China [20131202110008]
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Epithelial-mesenchymal transition (EMT) has been linked to cancer stem-like (CD44+) cell in the prostate cancer (PCa) metastasis. However, the molecular mechanism remains elusive. Here, we found EMT contributed to metastasis in PCa patients failed in androgen deprivation therapy (ADT). Castration TRAMP model also proved PCa treated with ADT promoted EMT with increased CD44+ stem-like cells. Switched CD44+ cell to EMT cell is a key step for luminal PCa cell metastasis. Our results also suggested ADT might go through promoting TGF beta 1-CD44 signaling to enhance swift to EMT. Targeting CD44 with salinomycin and siRNA could inhibit cell transition and decrease PCa invasion. Together, cancer stem-like (CD44+) cells could be the initiator cells of EMT modulated by TGF beta 1-CD44 signaling. Combined therapy of ADT with anti-CD44 may become a new potential therapeutic approach to battle later stage PCa.
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