Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1

Apoptosis signal-regulating kinase-1 (ASK-1) is an important molecule for the pro-apoptotic signaling. ASK-1 also contributes to the cellular survival for many types of cells. Thus, ASK-1 has a broad range of biological activities depending on the cell type. The present study assessed the role(s) of...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oncology reports 2007-04, Vol.17 (4), p.781-786
Hauptverfasser: KUWAMURA, Hikaru, TOMINAGA, Kazunari, ICHIJO, Hidenori, ARAKAWA, Tetsuo, IWAO, Hiroshi, SHIOTA, Masayuki, ASHIDA, Reiko, NAKAO, Takafumi, SASAKI, Eiji, WATANABE, Toshio, FUJIWARA, Yasuhiro, OSHITANI, Nobuhide, HIGUCHI, Kazuhide
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 786
container_issue 4
container_start_page 781
container_title Oncology reports
container_volume 17
creator KUWAMURA, Hikaru
TOMINAGA, Kazunari
ICHIJO, Hidenori
ARAKAWA, Tetsuo
IWAO, Hiroshi
SHIOTA, Masayuki
ASHIDA, Reiko
NAKAO, Takafumi
SASAKI, Eiji
WATANABE, Toshio
FUJIWARA, Yasuhiro
OSHITANI, Nobuhide
HIGUCHI, Kazuhide
description Apoptosis signal-regulating kinase-1 (ASK-1) is an important molecule for the pro-apoptotic signaling. ASK-1 also contributes to the cellular survival for many types of cells. Thus, ASK-1 has a broad range of biological activities depending on the cell type. The present study assessed the role(s) of ASK-1 in colorectal cancer cells (HT-29) by using adenovirus vectors expressing wild-type (WT)-ASK-1 or dominant-negative (DN) mutant of ASK-1 and recombinant adenovirus containing the bacterial beta-galactosidase gene (Ad-LacZ), a negative control for Ad-DN-ASK-1. Selective phosphorylation of ASK-1 at Thr 845, a kinase domain site, but not Ser 83 nor 967 sites was induced by serum stimulation in a time-dependent manner. Transfection with Ad-DN-ASK-1 inhibited the serum-induced phosphorylation of p38 mitogen-activated protein kinase, a downstream molecule of ASK-1. Transfection with Ad-DN-ASK-1 diminished the serum-induced cell proliferation in a dose-dependent manner, whereas WT-ASK-1 increased it. Apoptosis assessed by Hoechst staining was induced in the Ad-DN-ASK-1 treated cells. In vivo transfection of Ad-DN-ASK-1 into tumor xenografts of HT-29 cells in nude mice significantly decreased the tumor volume on day 29. Cleaved caspase-3 was found in the tumors of DN-ASK-1 treated mice. We obtained the first evidence that DN-ASK-1 transfection exerted significant antitumor effects on colon cancer mediated by apoptosis.
doi_str_mv 10.3892/or.17.4.781
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70257295</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70257295</sourcerecordid><originalsourceid>FETCH-LOGICAL-c312t-7b6232443e3fa6122d510c7570a6ff232d5553360092d2c3d29c2cfe805e57ce3</originalsourceid><addsrcrecordid>eNpF0MFKAzEQBuAgiq3Vk3fJRS-yNZlsNt2jFK1CwYuCt5Bmkza6Tdpkq_TtTWmlpxmYj2HmR-iakiEb1fAQ4pCKYTkUI3qC-lTUtICS0dPcE6AFY_yzhy5S-iIEBKnqc9SjgpXAKO-j9SSG326BnV-4metc8DhYrEObG628NhFr07YJz7a4i8ona_S_asLSeeW7wpu56tyPwWoVVl1ILuHk5l61RTTzTZtnfo6_s02moJfozKo2matDHaCP56f38UsxfZu8jh-nhWYUukLMKmBQlswwqyoK0HBKtOCCqMraPGo454xVhNTQgGYN1Bq0NSPCDRfasAG62-9dxbDemNTJpUu7X5Q3YZOkIMAF1DzD-z3UMaQUjZWr6JYqbiUlcpewDFFSIUuZE8765rB2M1ua5mgPkWZwewAqadXaHJp26ehGvK4hX_4HutmE2w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70257295</pqid></control><display><type>article</type><title>Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>KUWAMURA, Hikaru ; TOMINAGA, Kazunari ; ICHIJO, Hidenori ; ARAKAWA, Tetsuo ; IWAO, Hiroshi ; SHIOTA, Masayuki ; ASHIDA, Reiko ; NAKAO, Takafumi ; SASAKI, Eiji ; WATANABE, Toshio ; FUJIWARA, Yasuhiro ; OSHITANI, Nobuhide ; HIGUCHI, Kazuhide</creator><creatorcontrib>KUWAMURA, Hikaru ; TOMINAGA, Kazunari ; ICHIJO, Hidenori ; ARAKAWA, Tetsuo ; IWAO, Hiroshi ; SHIOTA, Masayuki ; ASHIDA, Reiko ; NAKAO, Takafumi ; SASAKI, Eiji ; WATANABE, Toshio ; FUJIWARA, Yasuhiro ; OSHITANI, Nobuhide ; HIGUCHI, Kazuhide</creatorcontrib><description>Apoptosis signal-regulating kinase-1 (ASK-1) is an important molecule for the pro-apoptotic signaling. ASK-1 also contributes to the cellular survival for many types of cells. Thus, ASK-1 has a broad range of biological activities depending on the cell type. The present study assessed the role(s) of ASK-1 in colorectal cancer cells (HT-29) by using adenovirus vectors expressing wild-type (WT)-ASK-1 or dominant-negative (DN) mutant of ASK-1 and recombinant adenovirus containing the bacterial beta-galactosidase gene (Ad-LacZ), a negative control for Ad-DN-ASK-1. Selective phosphorylation of ASK-1 at Thr 845, a kinase domain site, but not Ser 83 nor 967 sites was induced by serum stimulation in a time-dependent manner. Transfection with Ad-DN-ASK-1 inhibited the serum-induced phosphorylation of p38 mitogen-activated protein kinase, a downstream molecule of ASK-1. Transfection with Ad-DN-ASK-1 diminished the serum-induced cell proliferation in a dose-dependent manner, whereas WT-ASK-1 increased it. Apoptosis assessed by Hoechst staining was induced in the Ad-DN-ASK-1 treated cells. In vivo transfection of Ad-DN-ASK-1 into tumor xenografts of HT-29 cells in nude mice significantly decreased the tumor volume on day 29. Cleaved caspase-3 was found in the tumors of DN-ASK-1 treated mice. We obtained the first evidence that DN-ASK-1 transfection exerted significant antitumor effects on colon cancer mediated by apoptosis.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.17.4.781</identifier><identifier>PMID: 17342315</identifier><language>eng</language><publisher>Athens: S.n.</publisher><subject>Adenoviridae - genetics ; Animals ; Biological and medical sciences ; Caspase 3 - metabolism ; Colonic Neoplasms - therapy ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes, Dominant ; Genetic Therapy ; Genetic Vectors - genetics ; Humans ; MAP Kinase Kinase Kinase 5 - genetics ; MAP Kinase Kinase Kinase 5 - metabolism ; Medical sciences ; Mice ; Mice, Inbred Strains ; Mutation ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Transfection ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>Oncology reports, 2007-04, Vol.17 (4), p.781-786</ispartof><rights>2007 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=18599253$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17342315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KUWAMURA, Hikaru</creatorcontrib><creatorcontrib>TOMINAGA, Kazunari</creatorcontrib><creatorcontrib>ICHIJO, Hidenori</creatorcontrib><creatorcontrib>ARAKAWA, Tetsuo</creatorcontrib><creatorcontrib>IWAO, Hiroshi</creatorcontrib><creatorcontrib>SHIOTA, Masayuki</creatorcontrib><creatorcontrib>ASHIDA, Reiko</creatorcontrib><creatorcontrib>NAKAO, Takafumi</creatorcontrib><creatorcontrib>SASAKI, Eiji</creatorcontrib><creatorcontrib>WATANABE, Toshio</creatorcontrib><creatorcontrib>FUJIWARA, Yasuhiro</creatorcontrib><creatorcontrib>OSHITANI, Nobuhide</creatorcontrib><creatorcontrib>HIGUCHI, Kazuhide</creatorcontrib><title>Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Apoptosis signal-regulating kinase-1 (ASK-1) is an important molecule for the pro-apoptotic signaling. ASK-1 also contributes to the cellular survival for many types of cells. Thus, ASK-1 has a broad range of biological activities depending on the cell type. The present study assessed the role(s) of ASK-1 in colorectal cancer cells (HT-29) by using adenovirus vectors expressing wild-type (WT)-ASK-1 or dominant-negative (DN) mutant of ASK-1 and recombinant adenovirus containing the bacterial beta-galactosidase gene (Ad-LacZ), a negative control for Ad-DN-ASK-1. Selective phosphorylation of ASK-1 at Thr 845, a kinase domain site, but not Ser 83 nor 967 sites was induced by serum stimulation in a time-dependent manner. Transfection with Ad-DN-ASK-1 inhibited the serum-induced phosphorylation of p38 mitogen-activated protein kinase, a downstream molecule of ASK-1. Transfection with Ad-DN-ASK-1 diminished the serum-induced cell proliferation in a dose-dependent manner, whereas WT-ASK-1 increased it. Apoptosis assessed by Hoechst staining was induced in the Ad-DN-ASK-1 treated cells. In vivo transfection of Ad-DN-ASK-1 into tumor xenografts of HT-29 cells in nude mice significantly decreased the tumor volume on day 29. Cleaved caspase-3 was found in the tumors of DN-ASK-1 treated mice. We obtained the first evidence that DN-ASK-1 transfection exerted significant antitumor effects on colon cancer mediated by apoptosis.</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Caspase 3 - metabolism</subject><subject>Colonic Neoplasms - therapy</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes, Dominant</subject><subject>Genetic Therapy</subject><subject>Genetic Vectors - genetics</subject><subject>Humans</subject><subject>MAP Kinase Kinase Kinase 5 - genetics</subject><subject>MAP Kinase Kinase Kinase 5 - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mutation</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Transfection</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0MFKAzEQBuAgiq3Vk3fJRS-yNZlsNt2jFK1CwYuCt5Bmkza6Tdpkq_TtTWmlpxmYj2HmR-iakiEb1fAQ4pCKYTkUI3qC-lTUtICS0dPcE6AFY_yzhy5S-iIEBKnqc9SjgpXAKO-j9SSG326BnV-4metc8DhYrEObG628NhFr07YJz7a4i8ona_S_asLSeeW7wpu56tyPwWoVVl1ILuHk5l61RTTzTZtnfo6_s02moJfozKo2matDHaCP56f38UsxfZu8jh-nhWYUukLMKmBQlswwqyoK0HBKtOCCqMraPGo454xVhNTQgGYN1Bq0NSPCDRfasAG62-9dxbDemNTJpUu7X5Q3YZOkIMAF1DzD-z3UMaQUjZWr6JYqbiUlcpewDFFSIUuZE8765rB2M1ua5mgPkWZwewAqadXaHJp26ehGvK4hX_4HutmE2w</recordid><startdate>20070401</startdate><enddate>20070401</enddate><creator>KUWAMURA, Hikaru</creator><creator>TOMINAGA, Kazunari</creator><creator>ICHIJO, Hidenori</creator><creator>ARAKAWA, Tetsuo</creator><creator>IWAO, Hiroshi</creator><creator>SHIOTA, Masayuki</creator><creator>ASHIDA, Reiko</creator><creator>NAKAO, Takafumi</creator><creator>SASAKI, Eiji</creator><creator>WATANABE, Toshio</creator><creator>FUJIWARA, Yasuhiro</creator><creator>OSHITANI, Nobuhide</creator><creator>HIGUCHI, Kazuhide</creator><general>S.n.</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20070401</creationdate><title>Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1</title><author>KUWAMURA, Hikaru ; TOMINAGA, Kazunari ; ICHIJO, Hidenori ; ARAKAWA, Tetsuo ; IWAO, Hiroshi ; SHIOTA, Masayuki ; ASHIDA, Reiko ; NAKAO, Takafumi ; SASAKI, Eiji ; WATANABE, Toshio ; FUJIWARA, Yasuhiro ; OSHITANI, Nobuhide ; HIGUCHI, Kazuhide</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c312t-7b6232443e3fa6122d510c7570a6ff232d5553360092d2c3d29c2cfe805e57ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adenoviridae - genetics</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Caspase 3 - metabolism</topic><topic>Colonic Neoplasms - therapy</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes, Dominant</topic><topic>Genetic Therapy</topic><topic>Genetic Vectors - genetics</topic><topic>Humans</topic><topic>MAP Kinase Kinase Kinase 5 - genetics</topic><topic>MAP Kinase Kinase Kinase 5 - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mutation</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Transfection</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>online_resources</toplevel><creatorcontrib>KUWAMURA, Hikaru</creatorcontrib><creatorcontrib>TOMINAGA, Kazunari</creatorcontrib><creatorcontrib>ICHIJO, Hidenori</creatorcontrib><creatorcontrib>ARAKAWA, Tetsuo</creatorcontrib><creatorcontrib>IWAO, Hiroshi</creatorcontrib><creatorcontrib>SHIOTA, Masayuki</creatorcontrib><creatorcontrib>ASHIDA, Reiko</creatorcontrib><creatorcontrib>NAKAO, Takafumi</creatorcontrib><creatorcontrib>SASAKI, Eiji</creatorcontrib><creatorcontrib>WATANABE, Toshio</creatorcontrib><creatorcontrib>FUJIWARA, Yasuhiro</creatorcontrib><creatorcontrib>OSHITANI, Nobuhide</creatorcontrib><creatorcontrib>HIGUCHI, Kazuhide</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KUWAMURA, Hikaru</au><au>TOMINAGA, Kazunari</au><au>ICHIJO, Hidenori</au><au>ARAKAWA, Tetsuo</au><au>IWAO, Hiroshi</au><au>SHIOTA, Masayuki</au><au>ASHIDA, Reiko</au><au>NAKAO, Takafumi</au><au>SASAKI, Eiji</au><au>WATANABE, Toshio</au><au>FUJIWARA, Yasuhiro</au><au>OSHITANI, Nobuhide</au><au>HIGUCHI, Kazuhide</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2007-04-01</date><risdate>2007</risdate><volume>17</volume><issue>4</issue><spage>781</spage><epage>786</epage><pages>781-786</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Apoptosis signal-regulating kinase-1 (ASK-1) is an important molecule for the pro-apoptotic signaling. ASK-1 also contributes to the cellular survival for many types of cells. Thus, ASK-1 has a broad range of biological activities depending on the cell type. The present study assessed the role(s) of ASK-1 in colorectal cancer cells (HT-29) by using adenovirus vectors expressing wild-type (WT)-ASK-1 or dominant-negative (DN) mutant of ASK-1 and recombinant adenovirus containing the bacterial beta-galactosidase gene (Ad-LacZ), a negative control for Ad-DN-ASK-1. Selective phosphorylation of ASK-1 at Thr 845, a kinase domain site, but not Ser 83 nor 967 sites was induced by serum stimulation in a time-dependent manner. Transfection with Ad-DN-ASK-1 inhibited the serum-induced phosphorylation of p38 mitogen-activated protein kinase, a downstream molecule of ASK-1. Transfection with Ad-DN-ASK-1 diminished the serum-induced cell proliferation in a dose-dependent manner, whereas WT-ASK-1 increased it. Apoptosis assessed by Hoechst staining was induced in the Ad-DN-ASK-1 treated cells. In vivo transfection of Ad-DN-ASK-1 into tumor xenografts of HT-29 cells in nude mice significantly decreased the tumor volume on day 29. Cleaved caspase-3 was found in the tumors of DN-ASK-1 treated mice. We obtained the first evidence that DN-ASK-1 transfection exerted significant antitumor effects on colon cancer mediated by apoptosis.</abstract><cop>Athens</cop><pub>S.n.</pub><pmid>17342315</pmid><doi>10.3892/or.17.4.781</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1021-335X
ispartof Oncology reports, 2007-04, Vol.17 (4), p.781-786
issn 1021-335X
1791-2431
language eng
recordid cdi_proquest_miscellaneous_70257295
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Adenoviridae - genetics
Animals
Biological and medical sciences
Caspase 3 - metabolism
Colonic Neoplasms - therapy
Gastroenterology. Liver. Pancreas. Abdomen
Genes, Dominant
Genetic Therapy
Genetic Vectors - genetics
Humans
MAP Kinase Kinase Kinase 5 - genetics
MAP Kinase Kinase Kinase 5 - metabolism
Medical sciences
Mice
Mice, Inbred Strains
Mutation
p38 Mitogen-Activated Protein Kinases - metabolism
Phosphorylation
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Transfection
Tumors
Xenograft Model Antitumor Assays
title Growth inhibition of colon cancer cells by transfection of dominant-negative apoptosis signal-regulating kinase-1
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T05%3A50%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Growth%20inhibition%20of%20colon%20cancer%20cells%20by%20transfection%20of%20dominant-negative%20apoptosis%20signal-regulating%20kinase-1&rft.jtitle=Oncology%20reports&rft.au=KUWAMURA,%20Hikaru&rft.date=2007-04-01&rft.volume=17&rft.issue=4&rft.spage=781&rft.epage=786&rft.pages=781-786&rft.issn=1021-335X&rft.eissn=1791-2431&rft_id=info:doi/10.3892/or.17.4.781&rft_dat=%3Cproquest_cross%3E70257295%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=70257295&rft_id=info:pmid/17342315&rfr_iscdi=true