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Natural killer cells suppress enzalutamide resistance and cell invasion in the castration resistant prostate cancer via targeting the androgen receptor splicing variant 7 (ARv7)
Abstract Despite the success of androgen-deprivation therapy (ADT) with the newly developed anti-androgen enzalutamide (Enz, also known as MDV3100) to suppress castration resistant prostate cancer (CRPC) in extending patient survival by an extra 4.8 months, eventually patients die with the developme...
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Published in: | Cancer letters 2017-07, Vol.398, p.62-69 |
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container_title | Cancer letters |
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creator | Lin, Shin-Jen Chou, Fu-Ju Li, Lei Lin, Chang-Yi Yeh, Shuyuan Chang, Chawnshang |
description | Abstract Despite the success of androgen-deprivation therapy (ADT) with the newly developed anti-androgen enzalutamide (Enz, also known as MDV3100) to suppress castration resistant prostate cancer (CRPC) in extending patient survival by an extra 4.8 months, eventually patients die with the development of Enz resistance that may involve the induction of the androgen receptor (AR) splicing variant ARv7. Here we identify an unrecognized role of Natural Killer (NK) cells in the prostate tumor microenvironment that can be better recruited to the CRPC cells to suppress ARv7 expression resulting in suppressing the Enz resistant CRPC cell growth and invasion. Mechanism dissection revealed that CRPC cells compared to normal prostate epithelial cells could recruit more NK cells that might then lead to alterations of the microRNA-34 and microRNA-449 to suppress both ARv7 expression and ARv7-induced EZH2 expression to suppress CRPC cell invasion. Together, these results identify a new potential therapy using recruited NK cells to better suppress the Enz resistance and cell invasion in CRPC at the later enzalutamide resistant stage. |
doi_str_mv | 10.1016/j.canlet.2017.03.035 |
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Here we identify an unrecognized role of Natural Killer (NK) cells in the prostate tumor microenvironment that can be better recruited to the CRPC cells to suppress ARv7 expression resulting in suppressing the Enz resistant CRPC cell growth and invasion. Mechanism dissection revealed that CRPC cells compared to normal prostate epithelial cells could recruit more NK cells that might then lead to alterations of the microRNA-34 and microRNA-449 to suppress both ARv7 expression and ARv7-induced EZH2 expression to suppress CRPC cell invasion. Together, these results identify a new potential therapy using recruited NK cells to better suppress the Enz resistance and cell invasion in CRPC at the later enzalutamide resistant stage.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2017.03.035</identifier><identifier>PMID: 28373004</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>2-Mercaptoethanol ; Adhesion ; Adoptive transfer ; Agar ; Alternative Splicing ; American Type Culture Collection ; Androgen Antagonists - pharmacology ; Androgen receptors ; Androgens ; Animals ; Antibiotics ; Antibodies ; Antigens ; Antineoplastic Agents, Hormonal - pharmacology ; ARv7 ; Assaying ; Bicarbonates ; Biotechnology ; Bone marrow ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Chemotaxis, Leukocyte ; Clumps ; Coculture Techniques ; Cytotoxicity ; Down-Regulation ; Drug Resistance, Neoplasm ; Enhancer of Zeste Homolog 2 Protein - metabolism ; Enzalutamide ; Gene expression ; Gene silencing ; Glands ; Hematology, Oncology and Palliative Medicine ; Humans ; Immune response ; Immunoglobulins ; Immunotherapy ; Incidence ; Inhibition ; Inhibitors ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Lymph nodes ; Lymphocytes ; Lymphocytes B ; Lymphocytes, Tumor-Infiltrating - immunology ; Lymphocytes, Tumor-Infiltrating - metabolism ; Lysis ; Male ; Media ; Metastasis ; Mice, Nude ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Natural Killer cells ; Neoplasm Invasiveness ; Nucleic acids ; Pathogens ; Peptides ; Phenotype ; Phenylthiohydantoin - analogs & derivatives ; Phenylthiohydantoin - pharmacology ; Pore size ; Porosity ; Prostate cancer ; Prostatic Neoplasms, Castration-Resistant - drug therapy ; Prostatic Neoplasms, Castration-Resistant - immunology ; Prostatic Neoplasms, Castration-Resistant - metabolism ; Prostatic Neoplasms, Castration-Resistant - pathology ; Protein Isoforms ; Proteins ; Receptors, Androgen - drug effects ; Receptors, Androgen - metabolism ; Signal Transduction - drug effects ; Sodium ; Solidification ; Splicing ; Stem cells ; Time Factors ; Tumor cells ; Tumor Microenvironment ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer letters, 2017-07, Vol.398, p.62-69</ispartof><rights>Elsevier B.V.</rights><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier Limited Jul 10, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-87eec009255eb4af37b7faf2a4e2a981e5efbc693d254bc874ff7bd8f8585bcf3</citedby><cites>FETCH-LOGICAL-c445t-87eec009255eb4af37b7faf2a4e2a981e5efbc693d254bc874ff7bd8f8585bcf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28373004$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Shin-Jen</creatorcontrib><creatorcontrib>Chou, Fu-Ju</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Lin, Chang-Yi</creatorcontrib><creatorcontrib>Yeh, Shuyuan</creatorcontrib><creatorcontrib>Chang, Chawnshang</creatorcontrib><title>Natural killer cells suppress enzalutamide resistance and cell invasion in the castration resistant prostate cancer via targeting the androgen receptor splicing variant 7 (ARv7)</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract Despite the success of androgen-deprivation therapy (ADT) with the newly developed anti-androgen enzalutamide (Enz, also known as MDV3100) to suppress castration resistant prostate cancer (CRPC) in extending patient survival by an extra 4.8 months, eventually patients die with the development of Enz resistance that may involve the induction of the androgen receptor (AR) splicing variant ARv7. Here we identify an unrecognized role of Natural Killer (NK) cells in the prostate tumor microenvironment that can be better recruited to the CRPC cells to suppress ARv7 expression resulting in suppressing the Enz resistant CRPC cell growth and invasion. Mechanism dissection revealed that CRPC cells compared to normal prostate epithelial cells could recruit more NK cells that might then lead to alterations of the microRNA-34 and microRNA-449 to suppress both ARv7 expression and ARv7-induced EZH2 expression to suppress CRPC cell invasion. Together, these results identify a new potential therapy using recruited NK cells to better suppress the Enz resistance and cell invasion in CRPC at the later enzalutamide resistant stage.</description><subject>2-Mercaptoethanol</subject><subject>Adhesion</subject><subject>Adoptive transfer</subject><subject>Agar</subject><subject>Alternative Splicing</subject><subject>American Type Culture Collection</subject><subject>Androgen Antagonists - pharmacology</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Antineoplastic Agents, Hormonal - pharmacology</subject><subject>ARv7</subject><subject>Assaying</subject><subject>Bicarbonates</subject><subject>Biotechnology</subject><subject>Bone marrow</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotaxis, Leukocyte</subject><subject>Clumps</subject><subject>Coculture Techniques</subject><subject>Cytotoxicity</subject><subject>Down-Regulation</subject><subject>Drug Resistance, Neoplasm</subject><subject>Enhancer of Zeste Homolog 2 Protein - metabolism</subject><subject>Enzalutamide</subject><subject>Gene expression</subject><subject>Gene silencing</subject><subject>Glands</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunoglobulins</subject><subject>Immunotherapy</subject><subject>Incidence</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Lymph nodes</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes, Tumor-Infiltrating - immunology</subject><subject>Lymphocytes, Tumor-Infiltrating - metabolism</subject><subject>Lysis</subject><subject>Male</subject><subject>Media</subject><subject>Metastasis</subject><subject>Mice, Nude</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Natural Killer cells</subject><subject>Neoplasm Invasiveness</subject><subject>Nucleic acids</subject><subject>Pathogens</subject><subject>Peptides</subject><subject>Phenotype</subject><subject>Phenylthiohydantoin - analogs & derivatives</subject><subject>Phenylthiohydantoin - pharmacology</subject><subject>Pore size</subject><subject>Porosity</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms, Castration-Resistant - drug therapy</subject><subject>Prostatic Neoplasms, Castration-Resistant - immunology</subject><subject>Prostatic Neoplasms, Castration-Resistant - metabolism</subject><subject>Prostatic Neoplasms, Castration-Resistant - pathology</subject><subject>Protein Isoforms</subject><subject>Proteins</subject><subject>Receptors, Androgen - drug effects</subject><subject>Receptors, Androgen - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Sodium</subject><subject>Solidification</subject><subject>Splicing</subject><subject>Stem cells</subject><subject>Time Factors</subject><subject>Tumor cells</subject><subject>Tumor Microenvironment</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqFkl1vFCEUhonR2LX6D4wh8aZe7MoMsDA3Jk3jV9Jo4sc1OcOcWdmyMyMwk9R_5T8Uuq0mvTEhQA7P-3I4B0KeV2xTsWr7er-xMHhMm5pVasN4HvIBWVVa1WvVaPaQrBhnYs01lyfkSYx7xpgUSj4mJ7XmijMmVuT3J0hzAE-vnPcYqEXvI43zNAWMkeLwC_yc4OA6pDniYoLBIoWhu0GpGxaIbhzyhqYfSC3EFCCVyB2e6BTGvEnlNIsDXRzQBGGHyQ27G1n2C-MOi8jilMZA4-SdLccLBFdMFD07_7KoV0_Jox58xGe36yn5_u7tt4sP68vP7z9enF-urRAyrbVCtIw1tZTYCui5alUPfQ0Ca2h0hRL71m4b3tVStFYr0feq7XSvpZat7fkpOTv65ux_zhiTObhY3gwDjnM0ldai2opGNxl9eQ_dj3MYcnaZaqRotnUjMyWOlM3liAF7MwV3gHBtKmZKS83eHFtqSksN43kU2Ytb87k9YPdXdNfDDLw5ApirsTgMJlqHudCdy9VMphvd_264b2C9G5wFf4XXGP-9xcTaMPO1fKvyq6p8f50n_geO1c2O</recordid><startdate>20170710</startdate><enddate>20170710</enddate><creator>Lin, Shin-Jen</creator><creator>Chou, Fu-Ju</creator><creator>Li, Lei</creator><creator>Lin, Chang-Yi</creator><creator>Yeh, Shuyuan</creator><creator>Chang, Chawnshang</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20170710</creationdate><title>Natural killer cells suppress enzalutamide resistance and cell invasion in the castration resistant prostate cancer via targeting the androgen receptor splicing variant 7 (ARv7)</title><author>Lin, Shin-Jen ; Chou, Fu-Ju ; Li, Lei ; Lin, Chang-Yi ; Yeh, Shuyuan ; Chang, Chawnshang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-87eec009255eb4af37b7faf2a4e2a981e5efbc693d254bc874ff7bd8f8585bcf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>2-Mercaptoethanol</topic><topic>Adhesion</topic><topic>Adoptive transfer</topic><topic>Agar</topic><topic>Alternative Splicing</topic><topic>American Type Culture Collection</topic><topic>Androgen Antagonists - pharmacology</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Animals</topic><topic>Antibiotics</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Antineoplastic Agents, Hormonal - pharmacology</topic><topic>ARv7</topic><topic>Assaying</topic><topic>Bicarbonates</topic><topic>Biotechnology</topic><topic>Bone marrow</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotaxis, Leukocyte</topic><topic>Clumps</topic><topic>Coculture Techniques</topic><topic>Cytotoxicity</topic><topic>Down-Regulation</topic><topic>Drug Resistance, Neoplasm</topic><topic>Enhancer of Zeste Homolog 2 Protein - metabolism</topic><topic>Enzalutamide</topic><topic>Gene expression</topic><topic>Gene silencing</topic><topic>Glands</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunoglobulins</topic><topic>Immunotherapy</topic><topic>Incidence</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Lymph nodes</topic><topic>Lymphocytes</topic><topic>Lymphocytes B</topic><topic>Lymphocytes, Tumor-Infiltrating - immunology</topic><topic>Lymphocytes, Tumor-Infiltrating - metabolism</topic><topic>Lysis</topic><topic>Male</topic><topic>Media</topic><topic>Metastasis</topic><topic>Mice, Nude</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Natural Killer cells</topic><topic>Neoplasm Invasiveness</topic><topic>Nucleic acids</topic><topic>Pathogens</topic><topic>Peptides</topic><topic>Phenotype</topic><topic>Phenylthiohydantoin - analogs & derivatives</topic><topic>Phenylthiohydantoin - pharmacology</topic><topic>Pore size</topic><topic>Porosity</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms, Castration-Resistant - drug therapy</topic><topic>Prostatic Neoplasms, Castration-Resistant - immunology</topic><topic>Prostatic Neoplasms, Castration-Resistant - metabolism</topic><topic>Prostatic Neoplasms, Castration-Resistant - pathology</topic><topic>Protein Isoforms</topic><topic>Proteins</topic><topic>Receptors, Androgen - drug effects</topic><topic>Receptors, Androgen - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Sodium</topic><topic>Solidification</topic><topic>Splicing</topic><topic>Stem cells</topic><topic>Time Factors</topic><topic>Tumor cells</topic><topic>Tumor Microenvironment</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Shin-Jen</creatorcontrib><creatorcontrib>Chou, Fu-Ju</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Lin, Chang-Yi</creatorcontrib><creatorcontrib>Yeh, Shuyuan</creatorcontrib><creatorcontrib>Chang, Chawnshang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Shin-Jen</au><au>Chou, Fu-Ju</au><au>Li, Lei</au><au>Lin, Chang-Yi</au><au>Yeh, Shuyuan</au><au>Chang, Chawnshang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Natural killer cells suppress enzalutamide resistance and cell invasion in the castration resistant prostate cancer via targeting the androgen receptor splicing variant 7 (ARv7)</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2017-07-10</date><risdate>2017</risdate><volume>398</volume><spage>62</spage><epage>69</epage><pages>62-69</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract Despite the success of androgen-deprivation therapy (ADT) with the newly developed anti-androgen enzalutamide (Enz, also known as MDV3100) to suppress castration resistant prostate cancer (CRPC) in extending patient survival by an extra 4.8 months, eventually patients die with the development of Enz resistance that may involve the induction of the androgen receptor (AR) splicing variant ARv7. Here we identify an unrecognized role of Natural Killer (NK) cells in the prostate tumor microenvironment that can be better recruited to the CRPC cells to suppress ARv7 expression resulting in suppressing the Enz resistant CRPC cell growth and invasion. Mechanism dissection revealed that CRPC cells compared to normal prostate epithelial cells could recruit more NK cells that might then lead to alterations of the microRNA-34 and microRNA-449 to suppress both ARv7 expression and ARv7-induced EZH2 expression to suppress CRPC cell invasion. Together, these results identify a new potential therapy using recruited NK cells to better suppress the Enz resistance and cell invasion in CRPC at the later enzalutamide resistant stage.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>28373004</pmid><doi>10.1016/j.canlet.2017.03.035</doi><tpages>8</tpages></addata></record> |
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subjects | 2-Mercaptoethanol Adhesion Adoptive transfer Agar Alternative Splicing American Type Culture Collection Androgen Antagonists - pharmacology Androgen receptors Androgens Animals Antibiotics Antibodies Antigens Antineoplastic Agents, Hormonal - pharmacology ARv7 Assaying Bicarbonates Biotechnology Bone marrow Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Chemotaxis, Leukocyte Clumps Coculture Techniques Cytotoxicity Down-Regulation Drug Resistance, Neoplasm Enhancer of Zeste Homolog 2 Protein - metabolism Enzalutamide Gene expression Gene silencing Glands Hematology, Oncology and Palliative Medicine Humans Immune response Immunoglobulins Immunotherapy Incidence Inhibition Inhibitors Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Lymph nodes Lymphocytes Lymphocytes B Lymphocytes, Tumor-Infiltrating - immunology Lymphocytes, Tumor-Infiltrating - metabolism Lysis Male Media Metastasis Mice, Nude MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Natural Killer cells Neoplasm Invasiveness Nucleic acids Pathogens Peptides Phenotype Phenylthiohydantoin - analogs & derivatives Phenylthiohydantoin - pharmacology Pore size Porosity Prostate cancer Prostatic Neoplasms, Castration-Resistant - drug therapy Prostatic Neoplasms, Castration-Resistant - immunology Prostatic Neoplasms, Castration-Resistant - metabolism Prostatic Neoplasms, Castration-Resistant - pathology Protein Isoforms Proteins Receptors, Androgen - drug effects Receptors, Androgen - metabolism Signal Transduction - drug effects Sodium Solidification Splicing Stem cells Time Factors Tumor cells Tumor Microenvironment Xenograft Model Antitumor Assays |
title | Natural killer cells suppress enzalutamide resistance and cell invasion in the castration resistant prostate cancer via targeting the androgen receptor splicing variant 7 (ARv7) |
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