Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer

Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation o...

Full description

Saved in:
Bibliographic Details
Published in:Journal of Huazhong University of Science and Technology. Medical sciences 2004, Vol.24 (1), p.62-65
Main Author: 奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁
Format: Article
Language:English
Subjects:
Animals
cdc25 Phosphatases - metabolism
Cell Line, Tumor
DNA-Binding Proteins - metabolism
Female
Humans
Mice
Mice, Nude
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Proto-Oncogene Proteins c-myc - metabolism
Receptors, Transforming Growth Factor beta - metabolism
Signal Transduction
Smad4 Protein
Trans-Activators - metabolism
Transforming Growth Factor beta - pharmacology
信号通道
卵巢肿瘤
细胞周期
肿瘤转移
转化生长因子-β
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 65
container_issue 1
container_start_page 62
container_title Journal of Huazhong University of Science and Technology. Medical sciences
container_volume 24
creator 奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁
description Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF-β signaling transduction pathway such as C-myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF-β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C-myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi-quantitative RT-PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A genewas overexpressed with 88% (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20% (1/5) of non-tumorigenic cell lines (P
format article
fullrecord <record><control><sourceid>wanfang_jour_proqu</sourceid><recordid>TN_cdi_wanfang_journals_tjykdxxb_e200401017</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>9366661</cqvip_id><wanfj_id>tjykdxxb_e200401017</wanfj_id><sourcerecordid>tjykdxxb_e200401017</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1167-60a118df27c175b68fe4866fea2836ff719fdc408727a1510de10b764a5b2d143</originalsourceid><addsrcrecordid>eNo1kEtOIzEURUsIxK97Cy0zYYJKsutjV4at8GmkICJBj61XrueKQ8UOtguIxLz3w5g1sJXeApYCb-I3OPb1uTvZIZtMypyVdbGbdi6KnIqyPMiOQlhSWgteVPvZAasZrxlrDrPX803w2I8DROMscZrEBZL7q8v8443MXYgeFa6j8__f_92Z3sJgbE_mEBfPsCHGkikOA5kZi4GcozdP2BHt3YrMvVmB3xDnyQ1GCDEFKHL7BN5AugVWof-R7WkYAv78Oo-zv5cX99M_-ez26nr6e5YrlhRyTiH9tdOFUEzULW80Vg3nGqFoSq61YBPdqYo2ohCQ1GiHjLaCV1C3Rceq8jg72777DFaD7eXSjT6pBBmXm4fu5aWVWFBaUUaZSPTpll579zhiiHJlgkqaYNGNQaY4nqqsE_jrCxzbFXZyvVWW3-0m4GQLqIWz_WNqTragHrQZUE5KnoaVnwbShFY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71960055</pqid></control><display><type>article</type><title>Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer</title><source>Springer Link</source><creator>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</creator><creatorcontrib>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</creatorcontrib><description>Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF-β signaling transduction pathway such as C-myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF-β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C-myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi-quantitative RT-PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A genewas overexpressed with 88% (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20% (1/5) of non-tumorigenic cell lines (P&lt;0.05). C-myc was not overexpressed in any of these cell lines. The loss of sensitivity to TGF-β of cell lines derived from ovarian cancers may he related to a decreased expression of Smad4, which mediates TGF-β induced growthinhibition, and/or an overexpression of CDC25A. This overexpression of CDC25A correlates with increased tumorigenicity of ovarian cancer cell lines. The loss of sensitivity to TGF-β is not associated with a lack of TβR Ⅱ.</description><identifier>ISSN: 1672-0733</identifier><identifier>EISSN: 1993-1352</identifier><identifier>PMID: 15165118</identifier><language>eng</language><publisher>China: Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College,Huazhong University of Science and Technology, Wuhan 430030%Anderson Cancer Center, Taxras,USA%Southwestern Medical Center, Taxas, USA</publisher><subject>Animals ; cdc25 Phosphatases - metabolism ; Cell Line, Tumor ; DNA-Binding Proteins - metabolism ; Female ; Humans ; Mice ; Mice, Nude ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Proto-Oncogene Proteins c-myc - metabolism ; Receptors, Transforming Growth Factor beta - metabolism ; Signal Transduction ; Smad4 Protein ; Trans-Activators - metabolism ; Transforming Growth Factor beta - pharmacology ; 信号通道 ; 卵巢肿瘤 ; 细胞周期 ; 肿瘤转移 ; 转化生长因子-β</subject><ispartof>Journal of Huazhong University of Science and Technology. Medical sciences, 2004, Vol.24 (1), p.62-65</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85740A/85740A.jpg</thumbnail><link.rule.ids>314,776,780,4010</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15165118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</creatorcontrib><title>Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer</title><title>Journal of Huazhong University of Science and Technology. Medical sciences</title><addtitle>Journal of Zuazhong University of Science and Technology: Medical Edition</addtitle><description>Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF-β signaling transduction pathway such as C-myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF-β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C-myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi-quantitative RT-PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A genewas overexpressed with 88% (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20% (1/5) of non-tumorigenic cell lines (P&lt;0.05). C-myc was not overexpressed in any of these cell lines. The loss of sensitivity to TGF-β of cell lines derived from ovarian cancers may he related to a decreased expression of Smad4, which mediates TGF-β induced growthinhibition, and/or an overexpression of CDC25A. This overexpression of CDC25A correlates with increased tumorigenicity of ovarian cancer cell lines. The loss of sensitivity to TGF-β is not associated with a lack of TβR Ⅱ.</description><subject>Animals</subject><subject>cdc25 Phosphatases - metabolism</subject><subject>Cell Line, Tumor</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Receptors, Transforming Growth Factor beta - metabolism</subject><subject>Signal Transduction</subject><subject>Smad4 Protein</subject><subject>Trans-Activators - metabolism</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>信号通道</subject><subject>卵巢肿瘤</subject><subject>细胞周期</subject><subject>肿瘤转移</subject><subject>转化生长因子-β</subject><issn>1672-0733</issn><issn>1993-1352</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNo1kEtOIzEURUsIxK97Cy0zYYJKsutjV4at8GmkICJBj61XrueKQ8UOtguIxLz3w5g1sJXeApYCb-I3OPb1uTvZIZtMypyVdbGbdi6KnIqyPMiOQlhSWgteVPvZAasZrxlrDrPX803w2I8DROMscZrEBZL7q8v8443MXYgeFa6j8__f_92Z3sJgbE_mEBfPsCHGkikOA5kZi4GcozdP2BHt3YrMvVmB3xDnyQ1GCDEFKHL7BN5AugVWof-R7WkYAv78Oo-zv5cX99M_-ez26nr6e5YrlhRyTiH9tdOFUEzULW80Vg3nGqFoSq61YBPdqYo2ohCQ1GiHjLaCV1C3Rceq8jg72777DFaD7eXSjT6pBBmXm4fu5aWVWFBaUUaZSPTpll579zhiiHJlgkqaYNGNQaY4nqqsE_jrCxzbFXZyvVWW3-0m4GQLqIWz_WNqTragHrQZUE5KnoaVnwbShFY</recordid><startdate>2004</startdate><enddate>2004</enddate><creator>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</creator><general>Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College,Huazhong University of Science and Technology, Wuhan 430030%Anderson Cancer Center, Taxras,USA%Southwestern Medical Center, Taxas, USA</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>2004</creationdate><title>Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer</title><author>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1167-60a118df27c175b68fe4866fea2836ff719fdc408727a1510de10b764a5b2d143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>cdc25 Phosphatases - metabolism</topic><topic>Cell Line, Tumor</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Receptors, Transforming Growth Factor beta - metabolism</topic><topic>Signal Transduction</topic><topic>Smad4 Protein</topic><topic>Trans-Activators - metabolism</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>信号通道</topic><topic>卵巢肿瘤</topic><topic>细胞周期</topic><topic>肿瘤转移</topic><topic>转化生长因子-β</topic><toplevel>online_resources</toplevel><creatorcontrib>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Journal of Huazhong University of Science and Technology. Medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer</atitle><jtitle>Journal of Huazhong University of Science and Technology. Medical sciences</jtitle><addtitle>Journal of Zuazhong University of Science and Technology: Medical Edition</addtitle><date>2004</date><risdate>2004</risdate><volume>24</volume><issue>1</issue><spage>62</spage><epage>65</epage><pages>62-65</pages><issn>1672-0733</issn><eissn>1993-1352</eissn><abstract>Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF-β signaling transduction pathway such as C-myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF-β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C-myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi-quantitative RT-PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A genewas overexpressed with 88% (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20% (1/5) of non-tumorigenic cell lines (P&lt;0.05). C-myc was not overexpressed in any of these cell lines. The loss of sensitivity to TGF-β of cell lines derived from ovarian cancers may he related to a decreased expression of Smad4, which mediates TGF-β induced growthinhibition, and/or an overexpression of CDC25A. This overexpression of CDC25A correlates with increased tumorigenicity of ovarian cancer cell lines. The loss of sensitivity to TGF-β is not associated with a lack of TβR Ⅱ.</abstract><cop>China</cop><pub>Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College,Huazhong University of Science and Technology, Wuhan 430030%Anderson Cancer Center, Taxras,USA%Southwestern Medical Center, Taxas, USA</pub><pmid>15165118</pmid><tpages>4</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1672-0733
ispartof Journal of Huazhong University of Science and Technology. Medical sciences, 2004, Vol.24 (1), p.62-65
issn 1672-0733
1993-1352
language eng
recordid cdi_wanfang_journals_tjykdxxb_e200401017
source Springer Link
subjects Animals
cdc25 Phosphatases - metabolism
Cell Line, Tumor
DNA-Binding Proteins - metabolism
Female
Humans
Mice
Mice, Nude
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Proto-Oncogene Proteins c-myc - metabolism
Receptors, Transforming Growth Factor beta - metabolism
Signal Transduction
Smad4 Protein
Trans-Activators - metabolism
Transforming Growth Factor beta - pharmacology
信号通道
卵巢肿瘤
细胞周期
肿瘤转移
转化生长因子-β
title Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T19%3A27%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-wanfang_jour_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dysregulation%20of%20the%20TGF-%CE%B2%20Postreceptor%EF%BC%87Signaling%20Pathway%20in%20Cell%20Lines%20Derived%20from%20Primary%20or%20Metastatic%20Ovarian%20Cancer&rft.jtitle=Journal%20of%20Huazhong%20University%20of%20Science%20and%20Technology.%20Medical%20sciences&rft.au=%E5%A5%9A%E7%8E%B2%20%E8%83%A1%E4%BC%9F%20%E5%AD%9F%E5%8A%9B%20%E5%91%A8%E5%89%91%E5%B3%B0%20%E5%8D%A2%E8%BF%90%E8%90%8D%20%E7%8E%8B%E5%B8%B8%E7%8E%89%20%E9%A9%AC%E4%B8%81&rft.date=2004&rft.volume=24&rft.issue=1&rft.spage=62&rft.epage=65&rft.pages=62-65&rft.issn=1672-0733&rft.eissn=1993-1352&rft_id=info:doi/&rft_dat=%3Cwanfang_jour_proqu%3Etjykdxxb_e200401017%3C/wanfang_jour_proqu%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c1167-60a118df27c175b68fe4866fea2836ff719fdc408727a1510de10b764a5b2d143%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=71960055&rft_id=info:pmid/15165118&rft_cqvip_id=9366661&rft_wanfj_id=tjykdxxb_e200401017&rfr_iscdi=true