REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer

Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine...

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Published inScientific reports Vol. 7; no. 1; p. 42795
Main Authors Chang, Yi-Ting, Lin, Tzu-Ping, Campbell, Mel, Pan, Chin-Chen, Lee, Shu-Hui, Lee, Hsin-Chen, Yang, Muh-Hwa, Kung, Hsing-Jien, Chang, Pei-Ching
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 03.03.2017
Nature Publishing Group
Subjects
13/106
13/31
14/63
45/77
45/90
631/67/589/466
631/67/71
692/4025/1752
82/51
Humanities and Social Sciences
multidisciplinary
Science
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ISSN2045-2322
2045-2322
DOI10.1038/srep42795

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Abstract Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine (NE) cells is associated with CRPC. Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prostate cancer (PCa) cells via direct transcriptional repression of Twist1 and CD44. Specifically we show that short-term knockdown of REST induces NE differentiation of LNCaP cells. Long-term REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation. Overexpression of REST in hormone-refractory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere formation. Collectively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests that REST is a potential therapeutic target for CRPC.
AbstractList Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine (NE) cells is associated with CRPC. Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prostate cancer (PCa) cells via direct transcriptional repression of Twist1 and CD44. Specifically we show that short-term knockdown of REST induces NE differentiation of LNCaP cells. Long-term REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation. Overexpression of REST in hormone-refractory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere formation. Collectively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests that REST is a potential therapeutic target for CRPC.
Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine (NE) cells is associated with CRPC. Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prostate cancer (PCa) cells via direct transcriptional repression of Twist1 and CD44. Specifically we show that short-term knockdown of REST induces NE differentiation of LNCaP cells. Long-term REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation. Overexpression of REST in hormone-refractory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere formation. Collectively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests that REST is a potential therapeutic target for CRPC.Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only resistant to androgen ablation, chemo- and radiotherapy, but also highly metastatic. Increasing evidence suggests that enrichment of neuroendocrine (NE) cells is associated with CRPC. Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epithelial-mesenchymal transition (EMT) and stemness acquisition in NE differentiated prostate cancer (PCa) cells via direct transcriptional repression of Twist1 and CD44. Specifically we show that short-term knockdown of REST induces NE differentiation of LNCaP cells. Long-term REST knockdown enhanced the expression of Twist1 and CD44, cell migration and sphere formation. Overexpression of REST in hormone-refractory CWR22Rv1 PCa cells significantly reduces Twist1 and CD44 expression, cell migration and sphere formation. Collectively, our study uncovers REST in regulating EMT and stemness properties of NE PCa cells and suggests that REST is a potential therapeutic target for CRPC.
ArticleNumber 42795
Author Kung, Hsing-Jien
Campbell, Mel
Lee, Shu-Hui
Lin, Tzu-Ping
Chang, Pei-Ching
Pan, Chin-Chen
Chang, Yi-Ting
Lee, Hsin-Chen
Yang, Muh-Hwa
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  givenname: Mel
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  organization: UC Davis Comprehensive Cancer Center, University of California
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  organization: Institute of Clinical Medicine, National Yang-Ming University, Institute of Biotechnology in Medicine, National Yang-Ming University, Division of Hematology and Oncology, Department of Medicine, Taipei Veterans General Hospital, Genomics Research Center, Academia Sinica, Immunity and Inflammation Research Center, National Yang-Ming University, Genome Research Center, National Yang-Ming University
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  fullname: Kung, Hsing-Jien
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Snippet Castration-resistance prostate cancer (CRPC), also known as hormone-refractory prostate cancer (HRPC), requires immediate attention since it is not only...
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Title REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer
URI https://link.springer.com/article/10.1038/srep42795
https://www.ncbi.nlm.nih.gov/pubmed/28256535
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