uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells
Despite advances in radiotherapeutic and chemotherapeutic techniques and aggressive surgical resection, the prognosis of glioblastoma patients is dismal. Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resist...
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| Veröffentlicht in: | International journal of oncology 2012-08, Vol.41 (2), p.599-610 |
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| creator | ALAPATI, KIRANMAI GOPINATH, SREELATHA MALLA, RAMA RAO DASARI, VENKATA RAMESH RAO, JASTI S |
| description | Despite advances in radiotherapeutic and chemotherapeutic techniques and aggressive surgical resection, the prognosis of glioblastoma patients is dismal. Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resistant to therapy and are perhaps essential for the malignancy, may be cancer stem cells. The CD133 surface marker is commonly used to isolate these extremely resistant glioma-initiating cells (GICs). In the present study, GICs which tested positive for the CD133 marker (CD133+) were isolated from both the established U251 cell line and the 5310 xenograft glioma cell line to study the events related to the molecular pathogenesis of these cells. Simultaneous down-regulation of uPAR and cathepsin B by shRNA (pUC) treatment caused the disruption of radiation-induced complex formation of pPKC θ/δ, integrin β1 and PKC ζ, integrin β1 in glioma cells. Further, pUC treatment inhibited PKC/integrin signaling via FAK by causing disassociation of FAK and the cytoskeletal molecules vinculin and α-actinin. Also, we observed the inhibition of ERK phosphorylation. This inhibition was mediated by pUC and directed a negative feedback mechanism over the FAK signaling molecules, which led to an extensive reduction in the signal for cytoskeletal organization generating migratory arrest. Altogether, it can be hypothesized that knockdown of uPAR and cathepsin B using shRNA is an effective strategy for controlling highly invasive glioma cells and extremely resistant glioma-initiating cells. |
| doi_str_mv | 10.3892/ijo.2012.1496 |
| format | Article |
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Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resistant to therapy and are perhaps essential for the malignancy, may be cancer stem cells. The CD133 surface marker is commonly used to isolate these extremely resistant glioma-initiating cells (GICs). In the present study, GICs which tested positive for the CD133 marker (CD133+) were isolated from both the established U251 cell line and the 5310 xenograft glioma cell line to study the events related to the molecular pathogenesis of these cells. Simultaneous down-regulation of uPAR and cathepsin B by shRNA (pUC) treatment caused the disruption of radiation-induced complex formation of pPKC θ/δ, integrin β1 and PKC ζ, integrin β1 in glioma cells. Further, pUC treatment inhibited PKC/integrin signaling via FAK by causing disassociation of FAK and the cytoskeletal molecules vinculin and α-actinin. Also, we observed the inhibition of ERK phosphorylation. This inhibition was mediated by pUC and directed a negative feedback mechanism over the FAK signaling molecules, which led to an extensive reduction in the signal for cytoskeletal organization generating migratory arrest. Altogether, it can be hypothesized that knockdown of uPAR and cathepsin B using shRNA is an effective strategy for controlling highly invasive glioma cells and extremely resistant glioma-initiating cells.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2012.1496</identifier><identifier>PMID: 22641287</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Acetophenones - pharmacology ; Animals ; Antigens, Differentiation - metabolism ; Benzopyrans - pharmacology ; Brain cancer ; Breast cancer ; Cancer therapies ; cathepsin B ; Cathepsin B - genetics ; Cathepsin B - metabolism ; Cell adhesion & migration ; Cell Adhesion Molecules, Neuronal - metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Transformation, Neoplastic ; Cytoskeleton ; Cytoskeleton - metabolism ; Extracellular Matrix - metabolism ; Extracellular Matrix - physiology ; focal adhesion kinase ; Gene Expression - radiation effects ; Gene Knockdown Techniques ; glioblastoma stem cells ; Glioma ; Glioma - pathology ; Growth factors ; Humans ; Hypotheses ; Integrin beta1 - metabolism ; integrins ; Integrins - metabolism ; Kinases ; Mice ; Mice, Nude ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - radiation effects ; Penicillin ; Protein Binding ; protein kinase C ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; Proteins ; Radiation therapy ; Radiation Tolerance ; Receptors, Urokinase Plasminogen Activator - genetics ; Receptors, Urokinase Plasminogen Activator - metabolism ; RNA Interference ; RNA, Small Interfering - genetics ; Signal Transduction ; Spheroids, Cellular - metabolism ; Tumors ; uPAR ; vinculin ; Xenograft Model Antitumor Assays ; α-actinin</subject><ispartof>International journal of oncology, 2012-08, Vol.41 (2), p.599-610</ispartof><rights>Copyright © 2012, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2012</rights><rights>Copyright © 2012, Spandidos Publications 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-4e6bf6681cfa948939284775d07517a7be69c358ab4bfcdecb2323f5fa00593b3</citedby><cites>FETCH-LOGICAL-c513t-4e6bf6681cfa948939284775d07517a7be69c358ab4bfcdecb2323f5fa00593b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22641287$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ALAPATI, KIRANMAI</creatorcontrib><creatorcontrib>GOPINATH, SREELATHA</creatorcontrib><creatorcontrib>MALLA, RAMA RAO</creatorcontrib><creatorcontrib>DASARI, VENKATA RAMESH</creatorcontrib><creatorcontrib>RAO, JASTI S</creatorcontrib><title>uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Despite advances in radiotherapeutic and chemotherapeutic techniques and aggressive surgical resection, the prognosis of glioblastoma patients is dismal. Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resistant to therapy and are perhaps essential for the malignancy, may be cancer stem cells. The CD133 surface marker is commonly used to isolate these extremely resistant glioma-initiating cells (GICs). In the present study, GICs which tested positive for the CD133 marker (CD133+) were isolated from both the established U251 cell line and the 5310 xenograft glioma cell line to study the events related to the molecular pathogenesis of these cells. Simultaneous down-regulation of uPAR and cathepsin B by shRNA (pUC) treatment caused the disruption of radiation-induced complex formation of pPKC θ/δ, integrin β1 and PKC ζ, integrin β1 in glioma cells. Further, pUC treatment inhibited PKC/integrin signaling via FAK by causing disassociation of FAK and the cytoskeletal molecules vinculin and α-actinin. Also, we observed the inhibition of ERK phosphorylation. This inhibition was mediated by pUC and directed a negative feedback mechanism over the FAK signaling molecules, which led to an extensive reduction in the signal for cytoskeletal organization generating migratory arrest. Altogether, it can be hypothesized that knockdown of uPAR and cathepsin B using shRNA is an effective strategy for controlling highly invasive glioma cells and extremely resistant glioma-initiating cells.</description><subject>Acetophenones - pharmacology</subject><subject>Animals</subject><subject>Antigens, Differentiation - metabolism</subject><subject>Benzopyrans - pharmacology</subject><subject>Brain cancer</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>cathepsin B</subject><subject>Cathepsin B - genetics</subject><subject>Cathepsin B - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - metabolism</subject><subject>Extracellular Matrix - metabolism</subject><subject>Extracellular Matrix - physiology</subject><subject>focal adhesion kinase</subject><subject>Gene Expression - radiation effects</subject><subject>Gene Knockdown Techniques</subject><subject>glioblastoma stem cells</subject><subject>Glioma</subject><subject>Glioma - pathology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Integrin beta1 - metabolism</subject><subject>integrins</subject><subject>Integrins - metabolism</subject><subject>Kinases</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - radiation effects</subject><subject>Penicillin</subject><subject>Protein Binding</subject><subject>protein kinase C</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Radiation Tolerance</subject><subject>Receptors, Urokinase Plasminogen Activator - genetics</subject><subject>Receptors, Urokinase Plasminogen Activator - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal Transduction</subject><subject>Spheroids, Cellular - metabolism</subject><subject>Tumors</subject><subject>uPAR</subject><subject>vinculin</subject><subject>Xenograft Model Antitumor Assays</subject><subject>α-actinin</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpVkUtv1DAURiMEoqWwZIsssWDlqd-JN0hlxEut1ArB2nJsJ-OZjD3YDqh_gV-NoykjuvK17vG5vvqa5jVGK9pJcum3cUUQJivMpHjSnONWYkgYoU9rjbCEglF51rzIeYsQ4Rzh580ZIYJh0rXnzZ_57uob0MECo8vGHbIP4APYhWh2Nv4OwIeN733JIGnrdfExQB_sbJwFd9fr2i5uTLrU67Gsz7Mfg558GEGJoDqBuS8x79zkSgwgDmCcfNzr6vFlUVbQuGnKL5tng56ye_VwXjQ_Pn38vv4Cb24_f11f3UDDMS2QOdEPQnTYDFqyTlJJOta23KKW41a3vRPSUN7pnvWDsc70hBI68EEjxCXt6UXz_ug9zP3eWeNCSXpSh-T3Ot2rqL163Al-o8b4S1HWEdnxKnj7IEjx5-xyUds4p7pzVljSZZoQtFLwSJkUc05uOE3ASC3RqRqdWqJTS3SVf_P_t070v6wq8O4I5EPNy9uYT0w1QYYhIrCuKOlfjAClbA</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>ALAPATI, KIRANMAI</creator><creator>GOPINATH, SREELATHA</creator><creator>MALLA, RAMA RAO</creator><creator>DASARI, VENKATA RAMESH</creator><creator>RAO, JASTI S</creator><general>D.A. Spandidos</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><scope>5PM</scope></search><sort><creationdate>20120801</creationdate><title>uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells</title><author>ALAPATI, KIRANMAI ; GOPINATH, SREELATHA ; MALLA, RAMA RAO ; DASARI, VENKATA RAMESH ; RAO, JASTI S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-4e6bf6681cfa948939284775d07517a7be69c358ab4bfcdecb2323f5fa00593b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetophenones - pharmacology</topic><topic>Animals</topic><topic>Antigens, Differentiation - metabolism</topic><topic>Benzopyrans - pharmacology</topic><topic>Brain cancer</topic><topic>Breast cancer</topic><topic>Cancer therapies</topic><topic>cathepsin B</topic><topic>Cathepsin B - genetics</topic><topic>Cathepsin B - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cytoskeleton</topic><topic>Cytoskeleton - metabolism</topic><topic>Extracellular Matrix - metabolism</topic><topic>Extracellular Matrix - physiology</topic><topic>focal adhesion kinase</topic><topic>Gene Expression - radiation effects</topic><topic>Gene Knockdown Techniques</topic><topic>glioblastoma stem cells</topic><topic>Glioma</topic><topic>Glioma - pathology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Integrin beta1 - metabolism</topic><topic>integrins</topic><topic>Integrins - metabolism</topic><topic>Kinases</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - radiation effects</topic><topic>Penicillin</topic><topic>Protein Binding</topic><topic>protein kinase C</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Radiation Tolerance</topic><topic>Receptors, Urokinase Plasminogen Activator - genetics</topic><topic>Receptors, Urokinase Plasminogen Activator - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - genetics</topic><topic>Signal Transduction</topic><topic>Spheroids, Cellular - metabolism</topic><topic>Tumors</topic><topic>uPAR</topic><topic>vinculin</topic><topic>Xenograft Model Antitumor Assays</topic><topic>α-actinin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ALAPATI, KIRANMAI</creatorcontrib><creatorcontrib>GOPINATH, SREELATHA</creatorcontrib><creatorcontrib>MALLA, RAMA RAO</creatorcontrib><creatorcontrib>DASARI, VENKATA RAMESH</creatorcontrib><creatorcontrib>RAO, JASTI S</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>Proquest Nursing & Allied Health Source</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ALAPATI, KIRANMAI</au><au>GOPINATH, SREELATHA</au><au>MALLA, RAMA RAO</au><au>DASARI, VENKATA RAMESH</au><au>RAO, JASTI S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>41</volume><issue>2</issue><spage>599</spage><epage>610</epage><pages>599-610</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>Despite advances in radiotherapeutic and chemotherapeutic techniques and aggressive surgical resection, the prognosis of glioblastoma patients is dismal. Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resistant to therapy and are perhaps essential for the malignancy, may be cancer stem cells. The CD133 surface marker is commonly used to isolate these extremely resistant glioma-initiating cells (GICs). In the present study, GICs which tested positive for the CD133 marker (CD133+) were isolated from both the established U251 cell line and the 5310 xenograft glioma cell line to study the events related to the molecular pathogenesis of these cells. Simultaneous down-regulation of uPAR and cathepsin B by shRNA (pUC) treatment caused the disruption of radiation-induced complex formation of pPKC θ/δ, integrin β1 and PKC ζ, integrin β1 in glioma cells. Further, pUC treatment inhibited PKC/integrin signaling via FAK by causing disassociation of FAK and the cytoskeletal molecules vinculin and α-actinin. Also, we observed the inhibition of ERK phosphorylation. This inhibition was mediated by pUC and directed a negative feedback mechanism over the FAK signaling molecules, which led to an extensive reduction in the signal for cytoskeletal organization generating migratory arrest. Altogether, it can be hypothesized that knockdown of uPAR and cathepsin B using shRNA is an effective strategy for controlling highly invasive glioma cells and extremely resistant glioma-initiating cells.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>22641287</pmid><doi>10.3892/ijo.2012.1496</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2012-08, Vol.41 (2), p.599-610 |
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| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetophenones - pharmacology Animals Antigens, Differentiation - metabolism Benzopyrans - pharmacology Brain cancer Breast cancer Cancer therapies cathepsin B Cathepsin B - genetics Cathepsin B - metabolism Cell adhesion & migration Cell Adhesion Molecules, Neuronal - metabolism Cell Line, Tumor Cell Movement Cell Transformation, Neoplastic Cytoskeleton Cytoskeleton - metabolism Extracellular Matrix - metabolism Extracellular Matrix - physiology focal adhesion kinase Gene Expression - radiation effects Gene Knockdown Techniques glioblastoma stem cells Glioma Glioma - pathology Growth factors Humans Hypotheses Integrin beta1 - metabolism integrins Integrins - metabolism Kinases Mice Mice, Nude Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - radiation effects Penicillin Protein Binding protein kinase C Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Proteins Radiation therapy Radiation Tolerance Receptors, Urokinase Plasminogen Activator - genetics Receptors, Urokinase Plasminogen Activator - metabolism RNA Interference RNA, Small Interfering - genetics Signal Transduction Spheroids, Cellular - metabolism Tumors uPAR vinculin Xenograft Model Antitumor Assays α-actinin |
| title | uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells |
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