B7-H3 silencing inhibits tumor progression of mantle cell lymphoma and enhances chemosensitivity
B7-H3 (CD276), known as a member of B7 immunoregulatory family, is a type I transmembrane glycoprotein aberrantly expressed in numerous types of cancer and associated with poor prognosis. However, the role of B7-H3 in oncogenesis and chemosensitivity of mantle cell lymphoma (MCL) remains unknown. We...
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| Veröffentlicht in: | International journal of oncology 2015-06, Vol.46 (6), p.2562-2572 |
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| creator | ZHANG, WEI WANG, YANFANG WANG, JING DONG, FEI ZHU, MINGXIA WAN, WENLI LI, HAISHEN WU, FEIFEI YAN, XINXING KE, XIAOYAN |
| description | B7-H3 (CD276), known as a member of B7 immunoregulatory family, is a type I transmembrane glycoprotein aberrantly expressed in numerous types of cancer and associated with poor prognosis. However, the role of B7-H3 in oncogenesis and chemosensitivity of mantle cell lymphoma (MCL) remains unknown. We determined the effects of downregulating B7-H3 expression on tumor progression and the sensitivity of chemotherapeutic drug in mantle cell lymphoma. B7-H3 knockdown was performed using lentivirus transduction in the Maver and Z138 mantle cell lymphoma cell lines, respectively. The effects of B7-H3 on cell proliferation, cycle, migration and invasion were investigated by CCK-8 assay, methyl cellulose colony forming assay, PI staining, and Transwell assays in vitro. By establishing Maver and Z138 xenograft models, the effects of B7-H3 on tumorigenicity were observed, and Ki-67 and PCNA was detected by immunohistochemistry. The downregulation of B7-H3 significantly decreased tumor proliferation in MCL in vitro and in vivo. In the B7-H3 knockdown groups of Maver and Z138 xenograft models, the mean inhibition rate of tumor growth was 59.1 and 65.0% (p=0.010 and 0.003), and the expression of both Ki-67 and PCNA were significantly lower, respectively. After B7-H3 silencing, the cell cycles of Maver and Z138 were both arrested at G0/G1 phase, and the cell migration rates and invasion capacity were decreased as well. Moreover, the impacts of B7-H3 RNAi on the antitumor effect of chemotherapy drugs were determined with CCK-8 and Annexin V-FITC/PI assays in vitro and with xenograft models in vivo. The silencing of B7-H3 increased the sensitivity of Maver and Z138 cells to rituximab and bendamustine and enhanced the drug-induced apoptosis, respectively. Our study demonstrates for the first time that B7-H3 promotes mantle cell lymphoma progression and B7-H3 knockdown significantly enhances the chemosensitivity. This may provide a new therapeutic approach to mantle cell lymphoma. |
| doi_str_mv | 10.3892/ijo.2015.2962 |
| format | Article |
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However, the role of B7-H3 in oncogenesis and chemosensitivity of mantle cell lymphoma (MCL) remains unknown. We determined the effects of downregulating B7-H3 expression on tumor progression and the sensitivity of chemotherapeutic drug in mantle cell lymphoma. B7-H3 knockdown was performed using lentivirus transduction in the Maver and Z138 mantle cell lymphoma cell lines, respectively. The effects of B7-H3 on cell proliferation, cycle, migration and invasion were investigated by CCK-8 assay, methyl cellulose colony forming assay, PI staining, and Transwell assays in vitro. By establishing Maver and Z138 xenograft models, the effects of B7-H3 on tumorigenicity were observed, and Ki-67 and PCNA was detected by immunohistochemistry. The downregulation of B7-H3 significantly decreased tumor proliferation in MCL in vitro and in vivo. In the B7-H3 knockdown groups of Maver and Z138 xenograft models, the mean inhibition rate of tumor growth was 59.1 and 65.0% (p=0.010 and 0.003), and the expression of both Ki-67 and PCNA were significantly lower, respectively. After B7-H3 silencing, the cell cycles of Maver and Z138 were both arrested at G0/G1 phase, and the cell migration rates and invasion capacity were decreased as well. Moreover, the impacts of B7-H3 RNAi on the antitumor effect of chemotherapy drugs were determined with CCK-8 and Annexin V-FITC/PI assays in vitro and with xenograft models in vivo. The silencing of B7-H3 increased the sensitivity of Maver and Z138 cells to rituximab and bendamustine and enhanced the drug-induced apoptosis, respectively. Our study demonstrates for the first time that B7-H3 promotes mantle cell lymphoma progression and B7-H3 knockdown significantly enhances the chemosensitivity. This may provide a new therapeutic approach to mantle cell lymphoma.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2015.2962</identifier><identifier>PMID: 25872657</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Animals ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - pharmacology ; Apoptosis ; B7 Antigens - genetics ; B7 Antigens - metabolism ; B7-H3 ; Bendamustine Hydrochloride - administration & dosage ; Bendamustine Hydrochloride - pharmacology ; Breast cancer ; Cancer ; cancer gene therapy ; Cancer therapies ; Care and treatment ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; chemosensitivity ; Chemotherapy ; Cloning ; Development and progression ; Diagnosis ; Disease Progression ; Female ; Flow cytometry ; Gene expression ; Gene Silencing ; Humans ; Immunoglobulins ; Immunohistochemistry ; Infrared imaging systems ; Lymphoma ; Lymphoma, Mantle-Cell - drug therapy ; Lymphoma, Mantle-Cell - genetics ; Lymphoma, Mantle-Cell - metabolism ; Mantle cell lymphoma ; Medical prognosis ; Melanoma ; Mice ; Monoclonal antibodies ; Neoplasms, Experimental ; Non-Hodgkin's lymphomas ; Pancreatic cancer ; Rituximab - administration & dosage ; Rituximab - pharmacology ; Targeted cancer therapy</subject><ispartof>International journal of oncology, 2015-06, Vol.46 (6), p.2562-2572</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c556t-c44163f5bdd2d848eea718e053206645f6544fb03237563965a8530b33836ec53</citedby><cites>FETCH-LOGICAL-c556t-c44163f5bdd2d848eea718e053206645f6544fb03237563965a8530b33836ec53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25872657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHANG, WEI</creatorcontrib><creatorcontrib>WANG, YANFANG</creatorcontrib><creatorcontrib>WANG, JING</creatorcontrib><creatorcontrib>DONG, FEI</creatorcontrib><creatorcontrib>ZHU, MINGXIA</creatorcontrib><creatorcontrib>WAN, WENLI</creatorcontrib><creatorcontrib>LI, HAISHEN</creatorcontrib><creatorcontrib>WU, FEIFEI</creatorcontrib><creatorcontrib>YAN, XINXING</creatorcontrib><creatorcontrib>KE, XIAOYAN</creatorcontrib><title>B7-H3 silencing inhibits tumor progression of mantle cell lymphoma and enhances chemosensitivity</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>B7-H3 (CD276), known as a member of B7 immunoregulatory family, is a type I transmembrane glycoprotein aberrantly expressed in numerous types of cancer and associated with poor prognosis. However, the role of B7-H3 in oncogenesis and chemosensitivity of mantle cell lymphoma (MCL) remains unknown. We determined the effects of downregulating B7-H3 expression on tumor progression and the sensitivity of chemotherapeutic drug in mantle cell lymphoma. B7-H3 knockdown was performed using lentivirus transduction in the Maver and Z138 mantle cell lymphoma cell lines, respectively. The effects of B7-H3 on cell proliferation, cycle, migration and invasion were investigated by CCK-8 assay, methyl cellulose colony forming assay, PI staining, and Transwell assays in vitro. By establishing Maver and Z138 xenograft models, the effects of B7-H3 on tumorigenicity were observed, and Ki-67 and PCNA was detected by immunohistochemistry. The downregulation of B7-H3 significantly decreased tumor proliferation in MCL in vitro and in vivo. In the B7-H3 knockdown groups of Maver and Z138 xenograft models, the mean inhibition rate of tumor growth was 59.1 and 65.0% (p=0.010 and 0.003), and the expression of both Ki-67 and PCNA were significantly lower, respectively. After B7-H3 silencing, the cell cycles of Maver and Z138 were both arrested at G0/G1 phase, and the cell migration rates and invasion capacity were decreased as well. Moreover, the impacts of B7-H3 RNAi on the antitumor effect of chemotherapy drugs were determined with CCK-8 and Annexin V-FITC/PI assays in vitro and with xenograft models in vivo. The silencing of B7-H3 increased the sensitivity of Maver and Z138 cells to rituximab and bendamustine and enhanced the drug-induced apoptosis, respectively. Our study demonstrates for the first time that B7-H3 promotes mantle cell lymphoma progression and B7-H3 knockdown significantly enhances the chemosensitivity. This may provide a new therapeutic approach to mantle cell lymphoma.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>B7 Antigens - genetics</subject><subject>B7 Antigens - metabolism</subject><subject>B7-H3</subject><subject>Bendamustine Hydrochloride - administration & dosage</subject><subject>Bendamustine Hydrochloride - pharmacology</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>cancer gene therapy</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>chemosensitivity</subject><subject>Chemotherapy</subject><subject>Cloning</subject><subject>Development and progression</subject><subject>Diagnosis</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Immunohistochemistry</subject><subject>Infrared imaging systems</subject><subject>Lymphoma</subject><subject>Lymphoma, Mantle-Cell - drug therapy</subject><subject>Lymphoma, Mantle-Cell - genetics</subject><subject>Lymphoma, Mantle-Cell - metabolism</subject><subject>Mantle cell lymphoma</subject><subject>Medical prognosis</subject><subject>Melanoma</subject><subject>Mice</subject><subject>Monoclonal antibodies</subject><subject>Neoplasms, Experimental</subject><subject>Non-Hodgkin's lymphomas</subject><subject>Pancreatic cancer</subject><subject>Rituximab - administration & dosage</subject><subject>Rituximab - pharmacology</subject><subject>Targeted cancer therapy</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc9rFDEYhgdRbK0evUpAsKes-T2ZYy3WCgUveo6ZzDc7WTLJOskU9r83y9bSguSQHJ73TfI9TfOekg3XHfvsd2nDCJUb1in2ojmnbUcxE4y_rGdCO6wE786aNznvCGFSEvq6OWNSt0zJ9rz5_aXFtxxlHyA6H7fIx8n3vmRU1jktaL-k7QI5-xRRGtFsYwmAHISAwmHeT2m2yMYBQZxsdJCRm2BOGWL2xd_7cnjbvBptyPDuYb9oft18_Xl9i-9-fPt-fXWHnZSqYCcEVXyU_TCwQQsNYFuqgUjOiFJCjkoKMfaEM95KxTslrZac9JxrrsBJftF8PPXWF_9ZIRezS-sS65WGdjXFOk6fUFsbwPg4prJYN_vszJVglGiuRVepzX-ougaYvUsRxjqu54FPTwIT2FCmnMJa6tjycxCfQLeknBcYzX7xs10OhhJz9GmqT3P0aY4-K__h4VdrP8PwSP8TWIHLE5D3VYMfUn5kahMWChOFmaxVfwH-zKVN</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>ZHANG, WEI</creator><creator>WANG, YANFANG</creator><creator>WANG, JING</creator><creator>DONG, FEI</creator><creator>ZHU, MINGXIA</creator><creator>WAN, WENLI</creator><creator>LI, HAISHEN</creator><creator>WU, FEIFEI</creator><creator>YAN, XINXING</creator><creator>KE, XIAOYAN</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20150601</creationdate><title>B7-H3 silencing inhibits tumor progression of mantle cell lymphoma and enhances chemosensitivity</title><author>ZHANG, WEI ; WANG, YANFANG ; WANG, JING ; DONG, FEI ; ZHU, MINGXIA ; WAN, WENLI ; LI, HAISHEN ; WU, FEIFEI ; YAN, XINXING ; KE, XIAOYAN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c556t-c44163f5bdd2d848eea718e053206645f6544fb03237563965a8530b33836ec53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antineoplastic Agents - administration & dosage</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>B7 Antigens - genetics</topic><topic>B7 Antigens - metabolism</topic><topic>B7-H3</topic><topic>Bendamustine Hydrochloride - administration & dosage</topic><topic>Bendamustine Hydrochloride - pharmacology</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>cancer gene therapy</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>chemosensitivity</topic><topic>Chemotherapy</topic><topic>Cloning</topic><topic>Development and progression</topic><topic>Diagnosis</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Immunohistochemistry</topic><topic>Infrared imaging systems</topic><topic>Lymphoma</topic><topic>Lymphoma, Mantle-Cell - drug therapy</topic><topic>Lymphoma, Mantle-Cell - genetics</topic><topic>Lymphoma, Mantle-Cell - metabolism</topic><topic>Mantle cell lymphoma</topic><topic>Medical prognosis</topic><topic>Melanoma</topic><topic>Mice</topic><topic>Monoclonal antibodies</topic><topic>Neoplasms, Experimental</topic><topic>Non-Hodgkin's lymphomas</topic><topic>Pancreatic cancer</topic><topic>Rituximab - administration & dosage</topic><topic>Rituximab - pharmacology</topic><topic>Targeted cancer therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHANG, WEI</creatorcontrib><creatorcontrib>WANG, YANFANG</creatorcontrib><creatorcontrib>WANG, JING</creatorcontrib><creatorcontrib>DONG, FEI</creatorcontrib><creatorcontrib>ZHU, MINGXIA</creatorcontrib><creatorcontrib>WAN, WENLI</creatorcontrib><creatorcontrib>LI, HAISHEN</creatorcontrib><creatorcontrib>WU, FEIFEI</creatorcontrib><creatorcontrib>YAN, XINXING</creatorcontrib><creatorcontrib>KE, XIAOYAN</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>British Nursing Database</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHANG, WEI</au><au>WANG, YANFANG</au><au>WANG, JING</au><au>DONG, FEI</au><au>ZHU, MINGXIA</au><au>WAN, WENLI</au><au>LI, HAISHEN</au><au>WU, FEIFEI</au><au>YAN, XINXING</au><au>KE, XIAOYAN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B7-H3 silencing inhibits tumor progression of mantle cell lymphoma and enhances chemosensitivity</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>46</volume><issue>6</issue><spage>2562</spage><epage>2572</epage><pages>2562-2572</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>B7-H3 (CD276), known as a member of B7 immunoregulatory family, is a type I transmembrane glycoprotein aberrantly expressed in numerous types of cancer and associated with poor prognosis. However, the role of B7-H3 in oncogenesis and chemosensitivity of mantle cell lymphoma (MCL) remains unknown. We determined the effects of downregulating B7-H3 expression on tumor progression and the sensitivity of chemotherapeutic drug in mantle cell lymphoma. B7-H3 knockdown was performed using lentivirus transduction in the Maver and Z138 mantle cell lymphoma cell lines, respectively. The effects of B7-H3 on cell proliferation, cycle, migration and invasion were investigated by CCK-8 assay, methyl cellulose colony forming assay, PI staining, and Transwell assays in vitro. By establishing Maver and Z138 xenograft models, the effects of B7-H3 on tumorigenicity were observed, and Ki-67 and PCNA was detected by immunohistochemistry. The downregulation of B7-H3 significantly decreased tumor proliferation in MCL in vitro and in vivo. In the B7-H3 knockdown groups of Maver and Z138 xenograft models, the mean inhibition rate of tumor growth was 59.1 and 65.0% (p=0.010 and 0.003), and the expression of both Ki-67 and PCNA were significantly lower, respectively. After B7-H3 silencing, the cell cycles of Maver and Z138 were both arrested at G0/G1 phase, and the cell migration rates and invasion capacity were decreased as well. Moreover, the impacts of B7-H3 RNAi on the antitumor effect of chemotherapy drugs were determined with CCK-8 and Annexin V-FITC/PI assays in vitro and with xenograft models in vivo. The silencing of B7-H3 increased the sensitivity of Maver and Z138 cells to rituximab and bendamustine and enhanced the drug-induced apoptosis, respectively. Our study demonstrates for the first time that B7-H3 promotes mantle cell lymphoma progression and B7-H3 knockdown significantly enhances the chemosensitivity. This may provide a new therapeutic approach to mantle cell lymphoma.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25872657</pmid><doi>10.3892/ijo.2015.2962</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2015-06, Vol.46 (6), p.2562-2572 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Animals Antineoplastic Agents - administration & dosage Antineoplastic Agents - pharmacology Apoptosis B7 Antigens - genetics B7 Antigens - metabolism B7-H3 Bendamustine Hydrochloride - administration & dosage Bendamustine Hydrochloride - pharmacology Breast cancer Cancer cancer gene therapy Cancer therapies Care and treatment Cell cycle Cell growth Cell Line, Tumor Cell Movement Cell Proliferation chemosensitivity Chemotherapy Cloning Development and progression Diagnosis Disease Progression Female Flow cytometry Gene expression Gene Silencing Humans Immunoglobulins Immunohistochemistry Infrared imaging systems Lymphoma Lymphoma, Mantle-Cell - drug therapy Lymphoma, Mantle-Cell - genetics Lymphoma, Mantle-Cell - metabolism Mantle cell lymphoma Medical prognosis Melanoma Mice Monoclonal antibodies Neoplasms, Experimental Non-Hodgkin's lymphomas Pancreatic cancer Rituximab - administration & dosage Rituximab - pharmacology Targeted cancer therapy |
| title | B7-H3 silencing inhibits tumor progression of mantle cell lymphoma and enhances chemosensitivity |
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