PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9
Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the effect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the effects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's ly...
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Veröffentlicht in: | Clinical and investigative medicine 2012-06, Vol.35 (3), p.E117-E125 |
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creator | Xiong, Jie Qin, Jian Zheng, Yingcheng Peng, Xiaofan Luo, Yixing Meng, Xiangyu |
description | Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the effect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the effects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's lymphoma cell line, Raji.
Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the effect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. The expression levels of matrix metalloproteinases -2and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.
HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Specific inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.
Our findings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. The migration and adherence invasion capacity of Raji cells could potentially be affected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma. |
doi_str_mv | 10.25011/cim.v35i3.16587 |
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Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the effect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. The expression levels of matrix metalloproteinases -2and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.
HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Specific inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.
Our findings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. The migration and adherence invasion capacity of Raji cells could potentially be affected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma.</description><identifier>ISSN: 1488-2353</identifier><identifier>EISSN: 1488-2353</identifier><identifier>DOI: 10.25011/cim.v35i3.16587</identifier><identifier>PMID: 22673314</identifier><identifier>CODEN: CNVMDL</identifier><language>eng</language><publisher>Canada: Canadian Society for Clinical Investigation</publisher><subject>Apoptosis - drug effects ; Apoptosis - physiology ; Blotting, Western ; Burkitt Lymphoma - enzymology ; Burkitt Lymphoma - physiopathology ; Cell adhesion & migration ; Cell Line, Tumor ; Cell Movement - physiology ; Flow Cytometry ; Fluorouracil - pharmacology ; Gene expression ; HEK293 Cells ; Humans ; Immunotherapy ; Lymphoma ; Matrix Metalloproteinase 2 - biosynthesis ; Matrix Metalloproteinase 9 - biosynthesis ; Proteins - physiology ; Real-Time Polymerase Chain Reaction ; RNA, Small Interfering ; Studies ; Up-Regulation</subject><ispartof>Clinical and investigative medicine, 2012-06, Vol.35 (3), p.E117-E125</ispartof><rights>Copyright Canadian Society for Clinical Investigation Jun 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c323t-ac8c41591fb2a97344cdae7edfbdd00ff44265f6b2e2b44de59e8e0090140c233</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22673314$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiong, Jie</creatorcontrib><creatorcontrib>Qin, Jian</creatorcontrib><creatorcontrib>Zheng, Yingcheng</creatorcontrib><creatorcontrib>Peng, Xiaofan</creatorcontrib><creatorcontrib>Luo, Yixing</creatorcontrib><creatorcontrib>Meng, Xiangyu</creatorcontrib><title>PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9</title><title>Clinical and investigative medicine</title><addtitle>Clin Invest Med</addtitle><description>Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the effect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the effects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's lymphoma cell line, Raji.
Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the effect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. The expression levels of matrix metalloproteinases -2and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.
HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Specific inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.
Our findings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. The migration and adherence invasion capacity of Raji cells could potentially be affected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma.</description><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Blotting, Western</subject><subject>Burkitt Lymphoma - enzymology</subject><subject>Burkitt Lymphoma - physiopathology</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - physiology</subject><subject>Flow Cytometry</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene expression</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Immunotherapy</subject><subject>Lymphoma</subject><subject>Matrix Metalloproteinase 2 - biosynthesis</subject><subject>Matrix Metalloproteinase 9 - biosynthesis</subject><subject>Proteins - physiology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>RNA, Small Interfering</subject><subject>Studies</subject><subject>Up-Regulation</subject><issn>1488-2353</issn><issn>1488-2353</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkTtPwzAURi0E4lHYmZAlBlhS_MxjBFQeEhIMMEdOctMa4jjYDqIzfxxTCkJM9nC-z_f6IHRIyZRJQulZrc30jUvNpzSVebaBdqnI84RxyTf_3HfQnvfPhBAm02Ib7TCWZpxTsYs-HmbXlODBWWMDeBwWgI2eOxW07bFt8WI0qscXo3vRIZx43C3NsLBG4Rq6zuNqicchcTAfuxjp56sCeB8ceL9uMCo4_Y4NBNV1Nr4UQPfKQ8Kw6hucFPtoq1Wdh4P1OUFPV7PHy5vk7v769vL8Lqk54yFRdV4LKgvaVkwVGReibhRk0LRV0xDStkKwVLZpxYBVQjQgC8iBkIJQQWrG-QSdfvfGGV5H8KE02n-toXqwoy8poUVKs4J_ocf_0Gc7uj5OFylG42dLkUaKfFO1s947aMvBaaPcMkLlSlAZBZUrQeVKUIwcrYvHykDzG_gxwj8BlqONvw</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Xiong, Jie</creator><creator>Qin, Jian</creator><creator>Zheng, Yingcheng</creator><creator>Peng, Xiaofan</creator><creator>Luo, Yixing</creator><creator>Meng, Xiangyu</creator><general>Canadian Society for Clinical Investigation</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FQ</scope><scope>8FV</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M3G</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120601</creationdate><title>PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9</title><author>Xiong, Jie ; Qin, Jian ; Zheng, Yingcheng ; Peng, Xiaofan ; Luo, Yixing ; Meng, Xiangyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c323t-ac8c41591fb2a97344cdae7edfbdd00ff44265f6b2e2b44de59e8e0090140c233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Blotting, Western</topic><topic>Burkitt Lymphoma - enzymology</topic><topic>Burkitt Lymphoma - physiopathology</topic><topic>Cell adhesion & migration</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - physiology</topic><topic>Flow Cytometry</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene expression</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Immunotherapy</topic><topic>Lymphoma</topic><topic>Matrix Metalloproteinase 2 - biosynthesis</topic><topic>Matrix Metalloproteinase 9 - biosynthesis</topic><topic>Proteins - physiology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Small Interfering</topic><topic>Studies</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiong, Jie</creatorcontrib><creatorcontrib>Qin, Jian</creatorcontrib><creatorcontrib>Zheng, Yingcheng</creatorcontrib><creatorcontrib>Peng, Xiaofan</creatorcontrib><creatorcontrib>Luo, Yixing</creatorcontrib><creatorcontrib>Meng, Xiangyu</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</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>Canadian Business & Current Affairs Database</collection><collection>Canadian Business & Current Affairs Database (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>CBCA Reference & Current Events</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and investigative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiong, Jie</au><au>Qin, Jian</au><au>Zheng, Yingcheng</au><au>Peng, Xiaofan</au><au>Luo, Yixing</au><au>Meng, Xiangyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9</atitle><jtitle>Clinical and investigative medicine</jtitle><addtitle>Clin Invest Med</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>35</volume><issue>3</issue><spage>E117</spage><epage>E125</epage><pages>E117-E125</pages><issn>1488-2353</issn><eissn>1488-2353</eissn><coden>CNVMDL</coden><abstract>Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the effect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the effects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's lymphoma cell line, Raji.
Apoptosis was induced by 5-fluorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the effect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. The expression levels of matrix metalloproteinases -2and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.
HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Specific inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.
Our findings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. The migration and adherence invasion capacity of Raji cells could potentially be affected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma.</abstract><cop>Canada</cop><pub>Canadian Society for Clinical Investigation</pub><pmid>22673314</pmid><doi>10.25011/cim.v35i3.16587</doi></addata></record> |
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subjects | Apoptosis - drug effects Apoptosis - physiology Blotting, Western Burkitt Lymphoma - enzymology Burkitt Lymphoma - physiopathology Cell adhesion & migration Cell Line, Tumor Cell Movement - physiology Flow Cytometry Fluorouracil - pharmacology Gene expression HEK293 Cells Humans Immunotherapy Lymphoma Matrix Metalloproteinase 2 - biosynthesis Matrix Metalloproteinase 9 - biosynthesis Proteins - physiology Real-Time Polymerase Chain Reaction RNA, Small Interfering Studies Up-Regulation |
title | PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9 |
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