Abstract
Research in the last decade has clearly revealed a critical role of prostate cancer stem cells (PCSCs) in prostate cancer (PC). Prostate stem cells (PSCs) reside in both basal and luminal layers, and are the target cells of oncogenic transformation, suggesting a role of PCSCs in PC initiation. Mutations in PTEN, TP53, and RB1 commonly occur in PC, particularly in metastasis and castration-resistant PC. The loss of PTEN together with Ras activation induces partial epithelial–mesenchymal transition (EMT), which is a major mechanism that confers plasticity to cancer stem cells (CSCs) and PCSCs, which contributes to metastasis. While PTEN inactivation leads to PC, it is not sufficient for metastasis, the loss of PTEN concurrently with the inactivation of both TP53 and RB1 empower lineage plasticity in PC cells, which substantially promotes PC metastasis and the conversion to PC adenocarcinoma to neuroendocrine PC (NEPC), demonstrating the essential function of TP53 and RB1 in the suppression of PCSCs. TP53 and RB1 suppress lineage plasticity through the inhibition of SOX2 expression. In this review, we will discuss the current evidence supporting a major role of PCSCs in PC initiation and metastasis, as well as the underlying mechanisms regulating PCSCs. These discussions will be developed along with the cancer stem cell (CSC) knowledge in other cancer types.
Highlights
Prostate cancer (PC) is the most common male malignancy and a major cause of cancer death in men in the developed world [1]
prostate cancer (PC) can with This the content stemiscells (PSCs) both layers originate from both basal and luminal epithelial cells, indicating that prostate cancer stem cells (PCSCs) can generated from and
PC develops from high-grade prostatic intraepithelial neoplasia (HGPIN), The cancer stem cell (CSC) model states that cancer stem cells (CSCs) are the driving force of cancer evolution and which progresses to locally invasive carcinoma and metastatic cancer [7,8]
Summary
Prostate cancer (PC) is the most common male malignancy and a major cause of cancer death in men in the developed world [1]. Cancers 2019, 11, x and luminal epithelial cells, indicating that PCSCs can be generated from either layer; this is consistent unique of cellprostate population defined as in prostate cancer[6]. PC can with This the content stemiscells (PSCs) both layers originate from both basal and luminal epithelial cells, indicating that PCSCs can generated from and. PC develops from high-grade prostatic intraepithelial neoplasia (HGPIN), The cancer stem cell (CSC) model states that CSCs are the driving force of cancer evolution and which progresses to locally invasive carcinoma and metastatic cancer [7,8]. It was initially observed that surgical castration and estrogen injection discovery ledintosignificant androgen tumor deprivation therapy as the standard treatment patients resulted regression in 15(ADT). PSC: prostate stem cells; CTCs: circulating tumor cells. (B) The mechanisms that regulate PCSC stemness will be discussed
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