Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer

Background Colorectal cancer (CRC) is the third leading cause of death from cancer worldwide. Immature colon carcinoma transcript-1 (ICT1) has been reported to be correlated with lung cancer; however, whether ICT1 is a functional gene in CRC, as well as the molecular mechanism underlying ICT1 mediat...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Annals of surgical oncology 2016-11, Vol.23 (12), p.3924-3933
Hauptverfasser: Lao, Xinyuan, Feng, Qingyang, He, Guodong, Ji, Meiling, Zhu, Dexiang, Xu, Pingping, Tang, Wentao, Xu, Jianmin, Qin, Xinyu
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 3933
container_issue 12
container_start_page 3924
container_title Annals of surgical oncology
container_volume 23
creator Lao, Xinyuan
Feng, Qingyang
He, Guodong
Ji, Meiling
Zhu, Dexiang
Xu, Pingping
Tang, Wentao
Xu, Jianmin
Qin, Xinyu
description Background Colorectal cancer (CRC) is the third leading cause of death from cancer worldwide. Immature colon carcinoma transcript-1 (ICT1) has been reported to be correlated with lung cancer; however, whether ICT1 is a functional gene in CRC, as well as the molecular mechanism underlying ICT1 mediation of colorectal-tumor formation, remains unknown. Methods The expression of ICT1 was firstly determined by using immunohistochemistry in 861 CRC specimens. The correlation of ICT1 expression with clinicopathological parameters and the survival rate was analyzed. Furthermore, we investigated the effect of ICT1 silencing on CRC cell proliferation and migration by MTT, colony formation, flow cytometry, and transwell in vitro. Results ICT1 is highly expressed in a cohort of human CRCs, and that higher ICT1 expression may lead to reduced overall survival rate of CRC. Likewise, ICT1 silencing lowered the cell viability through cell-cycle arrest, inhibited cell migration, and induced apoptosis in CRC. We further revealed a novel mechanism in which ICT1 promoted CRC growth via the intracellular AMPK, SAPK/JNK, and PARP signaling pathways. Conclusions Our data showed that ICT1 could be an important target for CRC diagnosis and treatment.
doi_str_mv 10.1245/s10434-016-5305-1
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1826717759</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1826717759</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-9b0286716ee643faeef0c8ac15e4dbc5344c66b91eec3eadfa7aeaff927fb52c3</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhiMEoqXwAFyQJS7lEPA4sZMcUVRgpUpUYnuOJt5JcZXYyzjZwkPwzjjaBSEkTh55vv-f0fxZ9hLkW1ClfhdBlkWZSzC5LqTO4VF2Djr9lKaGx6mWps4bZfRZ9izGeymhStjT7ExVJYDWcJ793EwTzguTaMMYvGiRrfNhQrFl9NGy2885iMtNu4U34ur7nilGt4KBmUacKYoHN38Vt37AQ2DsRxI3HO58iC4K9DvxZeGDO-AonBc3ODvy80mzjmSyc-q16C3x8-zJgGOkF6f3Irv9cLVtP-XXnz9u2vfXuS0qNedNL1VtKjBEpiwGJBqkrdGCpnLX23SB0hrTN0BkC8LdgBUSDkOjqqHXyhYX2eXRd8_h20Jx7iYXLY0jegpL7KBWyb6qdJPQ1_-g92Fhn7ZbKV0YLVWRKDhSlkOMTEO3Zzch_-hAdmtW3TGrLmXVrVl1kDSvTs5LP9Huj-J3OAlQRyCmlr8j_mv0f11_AaB5oRg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1825365023</pqid></control><display><type>article</type><title>Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Lao, Xinyuan ; Feng, Qingyang ; He, Guodong ; Ji, Meiling ; Zhu, Dexiang ; Xu, Pingping ; Tang, Wentao ; Xu, Jianmin ; Qin, Xinyu</creator><creatorcontrib>Lao, Xinyuan ; Feng, Qingyang ; He, Guodong ; Ji, Meiling ; Zhu, Dexiang ; Xu, Pingping ; Tang, Wentao ; Xu, Jianmin ; Qin, Xinyu</creatorcontrib><description>Background Colorectal cancer (CRC) is the third leading cause of death from cancer worldwide. Immature colon carcinoma transcript-1 (ICT1) has been reported to be correlated with lung cancer; however, whether ICT1 is a functional gene in CRC, as well as the molecular mechanism underlying ICT1 mediation of colorectal-tumor formation, remains unknown. Methods The expression of ICT1 was firstly determined by using immunohistochemistry in 861 CRC specimens. The correlation of ICT1 expression with clinicopathological parameters and the survival rate was analyzed. Furthermore, we investigated the effect of ICT1 silencing on CRC cell proliferation and migration by MTT, colony formation, flow cytometry, and transwell in vitro. Results ICT1 is highly expressed in a cohort of human CRCs, and that higher ICT1 expression may lead to reduced overall survival rate of CRC. Likewise, ICT1 silencing lowered the cell viability through cell-cycle arrest, inhibited cell migration, and induced apoptosis in CRC. We further revealed a novel mechanism in which ICT1 promoted CRC growth via the intracellular AMPK, SAPK/JNK, and PARP signaling pathways. Conclusions Our data showed that ICT1 could be an important target for CRC diagnosis and treatment.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-016-5305-1</identifier><identifier>PMID: 27411551</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Adenylate Kinase - metabolism ; Aged ; Apoptosis - genetics ; Carcinoma - genetics ; Carcinoma - metabolism ; Carcinoma - secondary ; Cell Movement - genetics ; Cell Proliferation - genetics ; Cell Survival - genetics ; Colorectal Cancer ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Female ; G2 Phase Cell Cycle Checkpoints - genetics ; Gene Silencing ; HCT116 Cells ; Humans ; Male ; MAP Kinase Signaling System ; Medicine ; Medicine &amp; Public Health ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Staging ; Oncology ; Poly(ADP-ribose) Polymerases - metabolism ; Prognosis ; Proteins - genetics ; Proteins - metabolism ; Surgery ; Surgical Oncology ; Survival Rate</subject><ispartof>Annals of surgical oncology, 2016-11, Vol.23 (12), p.3924-3933</ispartof><rights>Society of Surgical Oncology 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-9b0286716ee643faeef0c8ac15e4dbc5344c66b91eec3eadfa7aeaff927fb52c3</citedby><cites>FETCH-LOGICAL-c372t-9b0286716ee643faeef0c8ac15e4dbc5344c66b91eec3eadfa7aeaff927fb52c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-016-5305-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-016-5305-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27411551$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lao, Xinyuan</creatorcontrib><creatorcontrib>Feng, Qingyang</creatorcontrib><creatorcontrib>He, Guodong</creatorcontrib><creatorcontrib>Ji, Meiling</creatorcontrib><creatorcontrib>Zhu, Dexiang</creatorcontrib><creatorcontrib>Xu, Pingping</creatorcontrib><creatorcontrib>Tang, Wentao</creatorcontrib><creatorcontrib>Xu, Jianmin</creatorcontrib><creatorcontrib>Qin, Xinyu</creatorcontrib><title>Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background Colorectal cancer (CRC) is the third leading cause of death from cancer worldwide. Immature colon carcinoma transcript-1 (ICT1) has been reported to be correlated with lung cancer; however, whether ICT1 is a functional gene in CRC, as well as the molecular mechanism underlying ICT1 mediation of colorectal-tumor formation, remains unknown. Methods The expression of ICT1 was firstly determined by using immunohistochemistry in 861 CRC specimens. The correlation of ICT1 expression with clinicopathological parameters and the survival rate was analyzed. Furthermore, we investigated the effect of ICT1 silencing on CRC cell proliferation and migration by MTT, colony formation, flow cytometry, and transwell in vitro. Results ICT1 is highly expressed in a cohort of human CRCs, and that higher ICT1 expression may lead to reduced overall survival rate of CRC. Likewise, ICT1 silencing lowered the cell viability through cell-cycle arrest, inhibited cell migration, and induced apoptosis in CRC. We further revealed a novel mechanism in which ICT1 promoted CRC growth via the intracellular AMPK, SAPK/JNK, and PARP signaling pathways. Conclusions Our data showed that ICT1 could be an important target for CRC diagnosis and treatment.</description><subject>Adenylate Kinase - metabolism</subject><subject>Aged</subject><subject>Apoptosis - genetics</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - secondary</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Survival - genetics</subject><subject>Colorectal Cancer</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Female</subject><subject>G2 Phase Cell Cycle Checkpoints - genetics</subject><subject>Gene Silencing</subject><subject>HCT116 Cells</subject><subject>Humans</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Prognosis</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Survival Rate</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kcFu1DAQhiMEoqXwAFyQJS7lEPA4sZMcUVRgpUpUYnuOJt5JcZXYyzjZwkPwzjjaBSEkTh55vv-f0fxZ9hLkW1ClfhdBlkWZSzC5LqTO4VF2Djr9lKaGx6mWps4bZfRZ9izGeymhStjT7ExVJYDWcJ793EwTzguTaMMYvGiRrfNhQrFl9NGy2885iMtNu4U34ur7nilGt4KBmUacKYoHN38Vt37AQ2DsRxI3HO58iC4K9DvxZeGDO-AonBc3ODvy80mzjmSyc-q16C3x8-zJgGOkF6f3Irv9cLVtP-XXnz9u2vfXuS0qNedNL1VtKjBEpiwGJBqkrdGCpnLX23SB0hrTN0BkC8LdgBUSDkOjqqHXyhYX2eXRd8_h20Jx7iYXLY0jegpL7KBWyb6qdJPQ1_-g92Fhn7ZbKV0YLVWRKDhSlkOMTEO3Zzch_-hAdmtW3TGrLmXVrVl1kDSvTs5LP9Huj-J3OAlQRyCmlr8j_mv0f11_AaB5oRg</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Lao, Xinyuan</creator><creator>Feng, Qingyang</creator><creator>He, Guodong</creator><creator>Ji, Meiling</creator><creator>Zhu, Dexiang</creator><creator>Xu, Pingping</creator><creator>Tang, Wentao</creator><creator>Xu, Jianmin</creator><creator>Qin, Xinyu</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20161101</creationdate><title>Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer</title><author>Lao, Xinyuan ; Feng, Qingyang ; He, Guodong ; Ji, Meiling ; Zhu, Dexiang ; Xu, Pingping ; Tang, Wentao ; Xu, Jianmin ; Qin, Xinyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-9b0286716ee643faeef0c8ac15e4dbc5344c66b91eec3eadfa7aeaff927fb52c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenylate Kinase - metabolism</topic><topic>Aged</topic><topic>Apoptosis - genetics</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - metabolism</topic><topic>Carcinoma - secondary</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Survival - genetics</topic><topic>Colorectal Cancer</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Female</topic><topic>G2 Phase Cell Cycle Checkpoints - genetics</topic><topic>Gene Silencing</topic><topic>HCT116 Cells</topic><topic>Humans</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>Medicine</topic><topic>Medicine &amp; Public Health</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Prognosis</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Survival Rate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lao, Xinyuan</creatorcontrib><creatorcontrib>Feng, Qingyang</creatorcontrib><creatorcontrib>He, Guodong</creatorcontrib><creatorcontrib>Ji, Meiling</creatorcontrib><creatorcontrib>Zhu, Dexiang</creatorcontrib><creatorcontrib>Xu, Pingping</creatorcontrib><creatorcontrib>Tang, Wentao</creatorcontrib><creatorcontrib>Xu, Jianmin</creatorcontrib><creatorcontrib>Qin, Xinyu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lao, Xinyuan</au><au>Feng, Qingyang</au><au>He, Guodong</au><au>Ji, Meiling</au><au>Zhu, Dexiang</au><au>Xu, Pingping</au><au>Tang, Wentao</au><au>Xu, Jianmin</au><au>Qin, Xinyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>23</volume><issue>12</issue><spage>3924</spage><epage>3933</epage><pages>3924-3933</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background Colorectal cancer (CRC) is the third leading cause of death from cancer worldwide. Immature colon carcinoma transcript-1 (ICT1) has been reported to be correlated with lung cancer; however, whether ICT1 is a functional gene in CRC, as well as the molecular mechanism underlying ICT1 mediation of colorectal-tumor formation, remains unknown. Methods The expression of ICT1 was firstly determined by using immunohistochemistry in 861 CRC specimens. The correlation of ICT1 expression with clinicopathological parameters and the survival rate was analyzed. Furthermore, we investigated the effect of ICT1 silencing on CRC cell proliferation and migration by MTT, colony formation, flow cytometry, and transwell in vitro. Results ICT1 is highly expressed in a cohort of human CRCs, and that higher ICT1 expression may lead to reduced overall survival rate of CRC. Likewise, ICT1 silencing lowered the cell viability through cell-cycle arrest, inhibited cell migration, and induced apoptosis in CRC. We further revealed a novel mechanism in which ICT1 promoted CRC growth via the intracellular AMPK, SAPK/JNK, and PARP signaling pathways. Conclusions Our data showed that ICT1 could be an important target for CRC diagnosis and treatment.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>27411551</pmid><doi>10.1245/s10434-016-5305-1</doi><tpages>10</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1068-9265
ispartof Annals of surgical oncology, 2016-11, Vol.23 (12), p.3924-3933
issn 1068-9265
1534-4681
language eng
recordid cdi_proquest_miscellaneous_1826717759
source MEDLINE; Springer Nature - Complete Springer Journals
subjects Adenylate Kinase - metabolism
Aged
Apoptosis - genetics
Carcinoma - genetics
Carcinoma - metabolism
Carcinoma - secondary
Cell Movement - genetics
Cell Proliferation - genetics
Cell Survival - genetics
Colorectal Cancer
Colorectal Neoplasms - genetics
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
Female
G2 Phase Cell Cycle Checkpoints - genetics
Gene Silencing
HCT116 Cells
Humans
Male
MAP Kinase Signaling System
Medicine
Medicine & Public Health
Middle Aged
Neoplasm Invasiveness
Neoplasm Staging
Oncology
Poly(ADP-ribose) Polymerases - metabolism
Prognosis
Proteins - genetics
Proteins - metabolism
Surgery
Surgical Oncology
Survival Rate
title Immature Colon Carcinoma Transcript-1 (ICT1) Expression Correlates with Unfavorable Prognosis and Survival in Patients with Colorectal Cancer
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T01%3A31%3A58IST&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=Immature%20Colon%20Carcinoma%20Transcript-1%20(ICT1)%20Expression%20Correlates%20with%20Unfavorable%20Prognosis%20and%20Survival%20in%20Patients%20with%20Colorectal%20Cancer&rft.jtitle=Annals%20of%20surgical%20oncology&rft.au=Lao,%20Xinyuan&rft.date=2016-11-01&rft.volume=23&rft.issue=12&rft.spage=3924&rft.epage=3933&rft.pages=3924-3933&rft.issn=1068-9265&rft.eissn=1534-4681&rft_id=info:doi/10.1245/s10434-016-5305-1&rft_dat=%3Cproquest_cross%3E1826717759%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=1825365023&rft_id=info:pmid/27411551&rfr_iscdi=true