shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells
Purpose Breast cancer is the cause for highest number of cancer-related death among women worldwide. This study was focused on investigating the role of zinc-finger protein X-linked (ZFX) in human breast cancer. Methods Expression levels of ZFX were analyzed in 99 patients and four breast cancer cel...
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| Veröffentlicht in: | Cancer chemotherapy and pharmacology 2014-03, Vol.73 (3), p.569-576 |
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| container_title | Cancer chemotherapy and pharmacology |
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| creator | Yang, Hongjian Lu, Yue Zheng, Yabing Yu, Xingfei Xia, Xianghou He, Xiangming Feng, Weiliang Xing, Lei Ling, Zhiqiang |
| description | Purpose
Breast cancer is the cause for highest number of cancer-related death among women worldwide. This study was focused on investigating the role of zinc-finger protein X-linked (ZFX) in human breast cancer.
Methods
Expression levels of ZFX were analyzed in 99 patients and four breast cancer cell lines. Lentivirus-mediated RNA interference was applied to silence ZFX expression, and the effects of ZFX knockdown on the growth of breast cancer cells were investigated.
Results
The immunohistochemical expression of ZFX was higher in more advanced tumor tissues. ZFX was also overexpressed in multiple breast cancer cell lines. Knockdown of ZFX inhibited cell proliferation and colony formation of MCF-7 and MDA-MB-231 cells. Moreover, ZFX silencing resulted in cell cycle arrest at G0/G1 phase. Depletion of ZFX decreased the phosphorylation level of AKT and increased the phosphorylation level of ERK2 and the expression of cyclin D1, which is involved in cell survival and cell cycle regulation.
Conclusions
These findings suggest that ZFX plays an important role in breast cancer development and could be a potential therapeutic target for breast cancer. |
| doi_str_mv | 10.1007/s00280-014-2379-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1501834239</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1501834239</sourcerecordid><originalsourceid>FETCH-LOGICAL-c402t-cbb03f6411bb52336c67f71bc03159d24a1efd4a2886446ee4cfe5efb4d8ffca3</originalsourceid><addsrcrecordid>eNp1kU1LHEEQhhtJ0HX1B3gJAyLk0kl1d83XUURjYEkgKoiXpqenep1ldmbtnjnsv7fH3ZgQyKkO9VTVy1OMnQn4IgDyrwFAFsBBIJcqL_n2gM0EKsmhQPWBzUAh8jQHPGLHIawAAIVSh-xIImKRqXzG7sLzrx-XfE11Ywaqk9C01NmmWya9S55uHhMzDNSNb73hmZKN79vGkTdD03cTU3kyYUis6Sz5xFLbhhP20Zk20Om-ztnDzfX91S1f_Pz2_epywS2CHLitKlAuQyGqKpVKZTbLXS4qC0qkZS3RCHI1GlkUGWJGhNZRSq7CunDOGjVnn3d7Y6iXkcKg102YEpiO-jFokYIoFEpVRvT8H3TVj76L6SYKyigsnSixo6zvQ_Dk9MY3a-O3WoCejOudcR2N68m43saZT_vNYxUtvk_8VhyBiz1ggjWt89FUE_5wRVqWZfzXnMkdF2KrW5L_K-J_r78CILqYrA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1500908459</pqid></control><display><type>article</type><title>shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Yang, Hongjian ; Lu, Yue ; Zheng, Yabing ; Yu, Xingfei ; Xia, Xianghou ; He, Xiangming ; Feng, Weiliang ; Xing, Lei ; Ling, Zhiqiang</creator><creatorcontrib>Yang, Hongjian ; Lu, Yue ; Zheng, Yabing ; Yu, Xingfei ; Xia, Xianghou ; He, Xiangming ; Feng, Weiliang ; Xing, Lei ; Ling, Zhiqiang</creatorcontrib><description>Purpose
Breast cancer is the cause for highest number of cancer-related death among women worldwide. This study was focused on investigating the role of zinc-finger protein X-linked (ZFX) in human breast cancer.
Methods
Expression levels of ZFX were analyzed in 99 patients and four breast cancer cell lines. Lentivirus-mediated RNA interference was applied to silence ZFX expression, and the effects of ZFX knockdown on the growth of breast cancer cells were investigated.
Results
The immunohistochemical expression of ZFX was higher in more advanced tumor tissues. ZFX was also overexpressed in multiple breast cancer cell lines. Knockdown of ZFX inhibited cell proliferation and colony formation of MCF-7 and MDA-MB-231 cells. Moreover, ZFX silencing resulted in cell cycle arrest at G0/G1 phase. Depletion of ZFX decreased the phosphorylation level of AKT and increased the phosphorylation level of ERK2 and the expression of cyclin D1, which is involved in cell survival and cell cycle regulation.
Conclusions
These findings suggest that ZFX plays an important role in breast cancer development and could be a potential therapeutic target for breast cancer.</description><identifier>ISSN: 0344-5704</identifier><identifier>EISSN: 1432-0843</identifier><identifier>DOI: 10.1007/s00280-014-2379-y</identifier><identifier>PMID: 24448637</identifier><identifier>CODEN: CCPHDZ</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Antineoplastic agents ; Apoptosis - genetics ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Breast Neoplasms - therapy ; Cancer Research ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - pathology ; Carcinoma, Ductal, Breast - therapy ; Cell Cycle Checkpoints ; Cell Growth Processes - genetics ; Cell Line, Tumor ; Female ; Gene Knockdown Techniques ; Gynecology. Andrology. Obstetrics ; HEK293 Cells ; Humans ; Kruppel-Like Transcription Factors - biosynthesis ; Kruppel-Like Transcription Factors - deficiency ; Kruppel-Like Transcription Factors - genetics ; Mammary gland diseases ; MCF-7 Cells ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Molecular Targeted Therapy ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Oncology ; Original Article ; Pharmacology. Drug treatments ; Pharmacology/Toxicology ; RNA Interference ; RNA, Small Interfering - administration & dosage ; RNA, Small Interfering - genetics ; Transfection ; Tumors</subject><ispartof>Cancer chemotherapy and pharmacology, 2014-03, Vol.73 (3), p.569-576</ispartof><rights>Springer-Verlag Berlin Heidelberg 2014</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-cbb03f6411bb52336c67f71bc03159d24a1efd4a2886446ee4cfe5efb4d8ffca3</citedby><cites>FETCH-LOGICAL-c402t-cbb03f6411bb52336c67f71bc03159d24a1efd4a2886446ee4cfe5efb4d8ffca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00280-014-2379-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00280-014-2379-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28599984$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24448637$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Hongjian</creatorcontrib><creatorcontrib>Lu, Yue</creatorcontrib><creatorcontrib>Zheng, Yabing</creatorcontrib><creatorcontrib>Yu, Xingfei</creatorcontrib><creatorcontrib>Xia, Xianghou</creatorcontrib><creatorcontrib>He, Xiangming</creatorcontrib><creatorcontrib>Feng, Weiliang</creatorcontrib><creatorcontrib>Xing, Lei</creatorcontrib><creatorcontrib>Ling, Zhiqiang</creatorcontrib><title>shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells</title><title>Cancer chemotherapy and pharmacology</title><addtitle>Cancer Chemother Pharmacol</addtitle><addtitle>Cancer Chemother Pharmacol</addtitle><description>Purpose
Breast cancer is the cause for highest number of cancer-related death among women worldwide. This study was focused on investigating the role of zinc-finger protein X-linked (ZFX) in human breast cancer.
Methods
Expression levels of ZFX were analyzed in 99 patients and four breast cancer cell lines. Lentivirus-mediated RNA interference was applied to silence ZFX expression, and the effects of ZFX knockdown on the growth of breast cancer cells were investigated.
Results
The immunohistochemical expression of ZFX was higher in more advanced tumor tissues. ZFX was also overexpressed in multiple breast cancer cell lines. Knockdown of ZFX inhibited cell proliferation and colony formation of MCF-7 and MDA-MB-231 cells. Moreover, ZFX silencing resulted in cell cycle arrest at G0/G1 phase. Depletion of ZFX decreased the phosphorylation level of AKT and increased the phosphorylation level of ERK2 and the expression of cyclin D1, which is involved in cell survival and cell cycle regulation.
Conclusions
These findings suggest that ZFX plays an important role in breast cancer development and could be a potential therapeutic target for breast cancer.</description><subject>Antineoplastic agents</subject><subject>Apoptosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - therapy</subject><subject>Cancer Research</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Carcinoma, Ductal, Breast - therapy</subject><subject>Cell Cycle Checkpoints</subject><subject>Cell Growth Processes - genetics</subject><subject>Cell Line, Tumor</subject><subject>Female</subject><subject>Gene Knockdown Techniques</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Kruppel-Like Transcription Factors - biosynthesis</subject><subject>Kruppel-Like Transcription Factors - deficiency</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>Mammary gland diseases</subject><subject>MCF-7 Cells</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Molecular Targeted Therapy</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacology/Toxicology</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - administration & dosage</subject><subject>RNA, Small Interfering - genetics</subject><subject>Transfection</subject><subject>Tumors</subject><issn>0344-5704</issn><issn>1432-0843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1LHEEQhhtJ0HX1B3gJAyLk0kl1d83XUURjYEkgKoiXpqenep1ldmbtnjnsv7fH3ZgQyKkO9VTVy1OMnQn4IgDyrwFAFsBBIJcqL_n2gM0EKsmhQPWBzUAh8jQHPGLHIawAAIVSh-xIImKRqXzG7sLzrx-XfE11Ywaqk9C01NmmWya9S55uHhMzDNSNb73hmZKN79vGkTdD03cTU3kyYUis6Sz5xFLbhhP20Zk20Om-ztnDzfX91S1f_Pz2_epywS2CHLitKlAuQyGqKpVKZTbLXS4qC0qkZS3RCHI1GlkUGWJGhNZRSq7CunDOGjVnn3d7Y6iXkcKg102YEpiO-jFokYIoFEpVRvT8H3TVj76L6SYKyigsnSixo6zvQ_Dk9MY3a-O3WoCejOudcR2N68m43saZT_vNYxUtvk_8VhyBiz1ggjWt89FUE_5wRVqWZfzXnMkdF2KrW5L_K-J_r78CILqYrA</recordid><startdate>20140301</startdate><enddate>20140301</enddate><creator>Yang, Hongjian</creator><creator>Lu, Yue</creator><creator>Zheng, Yabing</creator><creator>Yu, Xingfei</creator><creator>Xia, Xianghou</creator><creator>He, Xiangming</creator><creator>Feng, Weiliang</creator><creator>Xing, Lei</creator><creator>Ling, Zhiqiang</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>20140301</creationdate><title>shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells</title><author>Yang, Hongjian ; Lu, Yue ; Zheng, Yabing ; Yu, Xingfei ; Xia, Xianghou ; He, Xiangming ; Feng, Weiliang ; Xing, Lei ; Ling, Zhiqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-cbb03f6411bb52336c67f71bc03159d24a1efd4a2886446ee4cfe5efb4d8ffca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Antineoplastic agents</topic><topic>Apoptosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - therapy</topic><topic>Cancer Research</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Carcinoma, Ductal, Breast - therapy</topic><topic>Cell Cycle Checkpoints</topic><topic>Cell Growth Processes - genetics</topic><topic>Cell Line, Tumor</topic><topic>Female</topic><topic>Gene Knockdown Techniques</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Kruppel-Like Transcription Factors - biosynthesis</topic><topic>Kruppel-Like Transcription Factors - deficiency</topic><topic>Kruppel-Like Transcription Factors - genetics</topic><topic>Mammary gland diseases</topic><topic>MCF-7 Cells</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Molecular Targeted Therapy</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacology/Toxicology</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - administration & dosage</topic><topic>RNA, Small Interfering - genetics</topic><topic>Transfection</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Hongjian</creatorcontrib><creatorcontrib>Lu, Yue</creatorcontrib><creatorcontrib>Zheng, Yabing</creatorcontrib><creatorcontrib>Yu, Xingfei</creatorcontrib><creatorcontrib>Xia, Xianghou</creatorcontrib><creatorcontrib>He, Xiangming</creatorcontrib><creatorcontrib>Feng, Weiliang</creatorcontrib><creatorcontrib>Xing, Lei</creatorcontrib><creatorcontrib>Ling, Zhiqiang</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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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 & Medical Complete (Alumni)</collection><collection>Health & 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>Cancer chemotherapy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Hongjian</au><au>Lu, Yue</au><au>Zheng, Yabing</au><au>Yu, Xingfei</au><au>Xia, Xianghou</au><au>He, Xiangming</au><au>Feng, Weiliang</au><au>Xing, Lei</au><au>Ling, Zhiqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells</atitle><jtitle>Cancer chemotherapy and pharmacology</jtitle><stitle>Cancer Chemother Pharmacol</stitle><addtitle>Cancer Chemother Pharmacol</addtitle><date>2014-03-01</date><risdate>2014</risdate><volume>73</volume><issue>3</issue><spage>569</spage><epage>576</epage><pages>569-576</pages><issn>0344-5704</issn><eissn>1432-0843</eissn><coden>CCPHDZ</coden><abstract>Purpose
Breast cancer is the cause for highest number of cancer-related death among women worldwide. This study was focused on investigating the role of zinc-finger protein X-linked (ZFX) in human breast cancer.
Methods
Expression levels of ZFX were analyzed in 99 patients and four breast cancer cell lines. Lentivirus-mediated RNA interference was applied to silence ZFX expression, and the effects of ZFX knockdown on the growth of breast cancer cells were investigated.
Results
The immunohistochemical expression of ZFX was higher in more advanced tumor tissues. ZFX was also overexpressed in multiple breast cancer cell lines. Knockdown of ZFX inhibited cell proliferation and colony formation of MCF-7 and MDA-MB-231 cells. Moreover, ZFX silencing resulted in cell cycle arrest at G0/G1 phase. Depletion of ZFX decreased the phosphorylation level of AKT and increased the phosphorylation level of ERK2 and the expression of cyclin D1, which is involved in cell survival and cell cycle regulation.
Conclusions
These findings suggest that ZFX plays an important role in breast cancer development and could be a potential therapeutic target for breast cancer.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>24448637</pmid><doi>10.1007/s00280-014-2379-y</doi><tpages>8</tpages></addata></record> |
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| subjects | Antineoplastic agents Apoptosis - genetics Biological and medical sciences Breast cancer Breast Neoplasms - genetics Breast Neoplasms - pathology Breast Neoplasms - therapy Cancer Research Carcinoma, Ductal, Breast - genetics Carcinoma, Ductal, Breast - pathology Carcinoma, Ductal, Breast - therapy Cell Cycle Checkpoints Cell Growth Processes - genetics Cell Line, Tumor Female Gene Knockdown Techniques Gynecology. Andrology. Obstetrics HEK293 Cells Humans Kruppel-Like Transcription Factors - biosynthesis Kruppel-Like Transcription Factors - deficiency Kruppel-Like Transcription Factors - genetics Mammary gland diseases MCF-7 Cells Medical sciences Medicine Medicine & Public Health Middle Aged Molecular Targeted Therapy Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Oncology Original Article Pharmacology. Drug treatments Pharmacology/Toxicology RNA Interference RNA, Small Interfering - administration & dosage RNA, Small Interfering - genetics Transfection Tumors |
| title | shRNA-mediated silencing of ZFX attenuated the proliferation of breast cancer cells |
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