Abstract
In prostate cancer (PCa), similar to many other cancers, distant organ metastasis symbolizes the beginning of the end disease, which eventually leads to cancer death. Many mechanisms have been identified in this process that can be rationalized into targeted therapy. Among them, epithelial-to-mesenchymal transition (EMT) is originally characterized as a critical step for cell trans-differentiation during embryo development and now recognized in promoting cancer cells invasiveness because of high mobility and migratory abilities of mesenchymal cells once converted from carcinoma cells. Nevertheless, the underlying pathways leading to EMT appear to be very diverse in different cancer types, which certainly represent a challenge for developing effective intervention. In this article, we have carefully reviewed the key factors involved in EMT of PCa with clinical correlation in hope to facilitate the development of new therapeutic strategy that is expected to reduce the disease mortality.
Highlights
The plasticity of cellular phenotypic transformation is fundamental to embryonic development.During gastrulation stage, the reprogramming process of epithelial-to-mesenchymal transition (EMT)mainly governs the phenotypic change of polarized ectodermal epithelial cells into migratory mesenchymal cells that constitute the mesodermal layer of the embryo [1]
This study suggests that initiation of EMT by BMP7 can be regulated through PI3K and ERK signaling in prostate cancer (PCa)
This study demonstrated a critical impact of YB-1 on EMT, MTA1 is a chromatin remodeler playing an important role in PCa invasiveness
Summary
The plasticity of cellular phenotypic transformation is fundamental to embryonic development. Studies using clinical specimen and tumor model demonstrated a significant elevation of MTA1 in highly aggressive PCa, and that loss of MTA1 diminishes PCa invasion, bone metastasis and angiogenesis [68,69,70] Overall, these studies demonstrated a significant role of MTA1 and YB-1 in the EMT of PCa leading to metastatic progression of the disease. Loss of the mTORC1 or mTORC2 complex components, Raptor or Rictor, leads to attenuation of PCa migration and invasion due to elevated E-cadherin and β-catenin expression and reduced mesenchymal markers such as N-cadherin and vimentin [71] It appears that paclitaxel-resistant PCa cells are invasive [21]; this is initiated by EMT via Notch-1 signaling and suppression of E-cadherin expression. This study implies that Notch-1 signaling facilitates the mesenchymal phenotype associated with the acquisition of chemo-resistance in PCa cells
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