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Heavy Chain Ferritin siRNA Delivered by Cationic Liposomes Increases Sensitivity of Cancer Cells to Chemotherapeutic Agents
Approximately half of all gliomas are resistant to chemotherapy, and new therapeutic strategies are urgently needed to treat this cancer. We hypothesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute requirement for high levels of iron to meet energy re...
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| Published in: | Cancer research (Chicago, Ill.) Ill.), 2011-03, Vol.71 (6), p.2240-2249 |
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| cited_by | cdi_FETCH-LOGICAL-c469t-df406433a26316457ec09111aef8f09e523197e1978a818cf7cf1f16f35036373 |
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| cites | cdi_FETCH-LOGICAL-c469t-df406433a26316457ec09111aef8f09e523197e1978a818cf7cf1f16f35036373 |
| container_end_page | 2249 |
| container_issue | 6 |
| container_start_page | 2240 |
| container_title | Cancer research (Chicago, Ill.) |
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| creator | XIAOLI LIU MADHANKUMAR, A. B SLAGLE-WEBB, Becky SHEEHAN, Jonas M SURGULADZE, Nodar CONNOR, James R |
| description | Approximately half of all gliomas are resistant to chemotherapy, and new therapeutic strategies are urgently needed to treat this cancer. We hypothesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute requirement for high levels of iron to meet energy requirements associated with their rapid growth. Ferritin is best known as an intracellular iron storage protein, but it also localizes to tumor cell nuclei where it seems to protect DNA from oxidative damage and to promote transcription. In this study, we hypothesize that silencing the H-ferritin (heavy chain ferritin) gene could increase tumor sensitivity to chemotoxins. To test this hypothesis, H-ferritin siRNA was delivered to several human cancer cell lines by using cationic liposomes (C-liposome). H-ferritin siRNA decreased protein expression by 80% within 48 hours, and this decrease was associated with more than 50% decrease in the LD(50) for DNA-alkylating agent carmustine (BCNU), which is commonly used to treat glioma in clinic. In a subcutaneous mouse model of human glioma, intratumoral injections of liposomes containing H-ferritin siRNA reduced the effective dose of BCNU needed for tumor suppression by more than 50%. A plasmid supercoil relaxation assay showed that H-ferritin specifically and directly protected DNA from BCNU treatment. H-ferritin siRNA additionally seemed to increase apoptosis in glioma cells in vitro upon H-ferritin knockdown. Overall, our results illustrate how silencing H-ferritin can effectively sensitize tumors to chemotherapy and also show the ability of C-liposomes to serve as a novel in vivo delivery tool for siRNAs. |
| doi_str_mv | 10.1158/0008-5472.CAN-10-1375 |
| format | article |
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B ; SLAGLE-WEBB, Becky ; SHEEHAN, Jonas M ; SURGULADZE, Nodar ; CONNOR, James R</creator><creatorcontrib>XIAOLI LIU ; MADHANKUMAR, A. B ; SLAGLE-WEBB, Becky ; SHEEHAN, Jonas M ; SURGULADZE, Nodar ; CONNOR, James R</creatorcontrib><description>Approximately half of all gliomas are resistant to chemotherapy, and new therapeutic strategies are urgently needed to treat this cancer. We hypothesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute requirement for high levels of iron to meet energy requirements associated with their rapid growth. Ferritin is best known as an intracellular iron storage protein, but it also localizes to tumor cell nuclei where it seems to protect DNA from oxidative damage and to promote transcription. In this study, we hypothesize that silencing the H-ferritin (heavy chain ferritin) gene could increase tumor sensitivity to chemotoxins. To test this hypothesis, H-ferritin siRNA was delivered to several human cancer cell lines by using cationic liposomes (C-liposome). H-ferritin siRNA decreased protein expression by 80% within 48 hours, and this decrease was associated with more than 50% decrease in the LD(50) for DNA-alkylating agent carmustine (BCNU), which is commonly used to treat glioma in clinic. In a subcutaneous mouse model of human glioma, intratumoral injections of liposomes containing H-ferritin siRNA reduced the effective dose of BCNU needed for tumor suppression by more than 50%. A plasmid supercoil relaxation assay showed that H-ferritin specifically and directly protected DNA from BCNU treatment. H-ferritin siRNA additionally seemed to increase apoptosis in glioma cells in vitro upon H-ferritin knockdown. Overall, our results illustrate how silencing H-ferritin can effectively sensitize tumors to chemotherapy and also show the ability of C-liposomes to serve as a novel in vivo delivery tool for siRNAs.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-10-1375</identifier><identifier>PMID: 21385903</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animal models ; Animals ; Antineoplastic agents ; Antineoplastic Agents, Alkylating - therapeutic use ; Apoferritins - chemistry ; Apoferritins - genetics ; Apoptosis ; Apoptosis - genetics ; Biological and medical sciences ; Blotting, Western ; Brain tumors ; Carmustine - therapeutic use ; Caspase 3 - metabolism ; Cations - chemistry ; Cell Line, Tumor ; Chemotherapy ; DNA ; DNA damage ; DNA, Neoplasm - chemistry ; DNA, Neoplasm - genetics ; DNA, Superhelical - chemistry ; DNA, Superhelical - genetics ; Dose-Response Relationship, Drug ; Down-Regulation ; Energy requirements ; Female ; Ferritin ; Glioma ; Glioma - drug therapy ; Glioma - genetics ; Glioma - pathology ; Glioma cells ; Homeostasis ; Humans ; Iron ; Liposomes ; Liposomes - chemistry ; Medical sciences ; Mice ; Mice, Nude ; Nuclei ; Nucleic Acid Conformation - drug effects ; Pharmacology. Drug treatments ; Plasmids ; RNA Interference ; RNA, Small Interfering - chemistry ; RNA, Small Interfering - genetics ; siRNA ; storage proteins ; Transcription ; Transfection ; Tumor cell lines ; Tumor cells ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer research (Chicago, Ill.), 2011-03, Vol.71 (6), p.2240-2249</ispartof><rights>2015 INIST-CNRS</rights><rights>2011 AACR.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-df406433a26316457ec09111aef8f09e523197e1978a818cf7cf1f16f35036373</citedby><cites>FETCH-LOGICAL-c469t-df406433a26316457ec09111aef8f09e523197e1978a818cf7cf1f16f35036373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24027301$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21385903$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>XIAOLI LIU</creatorcontrib><creatorcontrib>MADHANKUMAR, A. B</creatorcontrib><creatorcontrib>SLAGLE-WEBB, Becky</creatorcontrib><creatorcontrib>SHEEHAN, Jonas M</creatorcontrib><creatorcontrib>SURGULADZE, Nodar</creatorcontrib><creatorcontrib>CONNOR, James R</creatorcontrib><title>Heavy Chain Ferritin siRNA Delivered by Cationic Liposomes Increases Sensitivity of Cancer Cells to Chemotherapeutic Agents</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Approximately half of all gliomas are resistant to chemotherapy, and new therapeutic strategies are urgently needed to treat this cancer. We hypothesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute requirement for high levels of iron to meet energy requirements associated with their rapid growth. Ferritin is best known as an intracellular iron storage protein, but it also localizes to tumor cell nuclei where it seems to protect DNA from oxidative damage and to promote transcription. In this study, we hypothesize that silencing the H-ferritin (heavy chain ferritin) gene could increase tumor sensitivity to chemotoxins. To test this hypothesis, H-ferritin siRNA was delivered to several human cancer cell lines by using cationic liposomes (C-liposome). H-ferritin siRNA decreased protein expression by 80% within 48 hours, and this decrease was associated with more than 50% decrease in the LD(50) for DNA-alkylating agent carmustine (BCNU), which is commonly used to treat glioma in clinic. In a subcutaneous mouse model of human glioma, intratumoral injections of liposomes containing H-ferritin siRNA reduced the effective dose of BCNU needed for tumor suppression by more than 50%. A plasmid supercoil relaxation assay showed that H-ferritin specifically and directly protected DNA from BCNU treatment. H-ferritin siRNA additionally seemed to increase apoptosis in glioma cells in vitro upon H-ferritin knockdown. Overall, our results illustrate how silencing H-ferritin can effectively sensitize tumors to chemotherapy and also show the ability of C-liposomes to serve as a novel in vivo delivery tool for siRNAs.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents, Alkylating - therapeutic use</subject><subject>Apoferritins - chemistry</subject><subject>Apoferritins - genetics</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Brain tumors</subject><subject>Carmustine - therapeutic use</subject><subject>Caspase 3 - metabolism</subject><subject>Cations - chemistry</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA, Neoplasm - chemistry</subject><subject>DNA, Neoplasm - genetics</subject><subject>DNA, Superhelical - chemistry</subject><subject>DNA, Superhelical - genetics</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation</subject><subject>Energy requirements</subject><subject>Female</subject><subject>Ferritin</subject><subject>Glioma</subject><subject>Glioma - drug therapy</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Iron</subject><subject>Liposomes</subject><subject>Liposomes - chemistry</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Nuclei</subject><subject>Nucleic Acid Conformation - drug effects</subject><subject>Pharmacology. Drug treatments</subject><subject>Plasmids</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - chemistry</subject><subject>RNA, Small Interfering - genetics</subject><subject>siRNA</subject><subject>storage proteins</subject><subject>Transcription</subject><subject>Transfection</subject><subject>Tumor cell lines</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqFkVFPHCEUhYlpU7e2P0HDS-PTWO4AA_O4GbWabGxS7fME2UulmRlWYDfZ-OdldbWPfSBcyHcO5BxCjoGdAUj9nTGmKylUfdbNbypgFXAlD8gMJNeVEkJ-ILN35pB8TulvOUpg8hM5rIFr2TI-I09XaDZb2j0YP9FLjNHnMiT_62ZOz3HwG4y4pPeFMNmHyVu68KuQwoiJXk82okllusUpFeHG5y0NrrCTxUg7HIZEcyjuOIb8gNGscJ2Lx_wPTjl9IR-dGRJ-3e9H5PflxV13VS1-_rju5ovKiqbN1dIJ1gjOTd1waIRUaFkLAAaddqxFWXNoFZaljQZtnbIOHDSOS8YbrvgROX31XcXwuMaU-9EnWz5nJgzr1LdMCA1Mw39JLZXQXNSskPKVtDGkFNH1q-hHE7c9sH5XUL8Lv9-F35eCXm5LQUV3sn9hfT_i8l311kgBvu0Bk6wZXCxZ-vSPE6xWnAF_BsjNmEA</recordid><startdate>20110315</startdate><enddate>20110315</enddate><creator>XIAOLI LIU</creator><creator>MADHANKUMAR, A. 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Drug treatments</topic><topic>Plasmids</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - chemistry</topic><topic>RNA, Small Interfering - genetics</topic><topic>siRNA</topic><topic>storage proteins</topic><topic>Transcription</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>XIAOLI LIU</creatorcontrib><creatorcontrib>MADHANKUMAR, A. 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We hypothesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute requirement for high levels of iron to meet energy requirements associated with their rapid growth. Ferritin is best known as an intracellular iron storage protein, but it also localizes to tumor cell nuclei where it seems to protect DNA from oxidative damage and to promote transcription. In this study, we hypothesize that silencing the H-ferritin (heavy chain ferritin) gene could increase tumor sensitivity to chemotoxins. To test this hypothesis, H-ferritin siRNA was delivered to several human cancer cell lines by using cationic liposomes (C-liposome). H-ferritin siRNA decreased protein expression by 80% within 48 hours, and this decrease was associated with more than 50% decrease in the LD(50) for DNA-alkylating agent carmustine (BCNU), which is commonly used to treat glioma in clinic. In a subcutaneous mouse model of human glioma, intratumoral injections of liposomes containing H-ferritin siRNA reduced the effective dose of BCNU needed for tumor suppression by more than 50%. A plasmid supercoil relaxation assay showed that H-ferritin specifically and directly protected DNA from BCNU treatment. H-ferritin siRNA additionally seemed to increase apoptosis in glioma cells in vitro upon H-ferritin knockdown. Overall, our results illustrate how silencing H-ferritin can effectively sensitize tumors to chemotherapy and also show the ability of C-liposomes to serve as a novel in vivo delivery tool for siRNAs.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>21385903</pmid><doi>10.1158/0008-5472.CAN-10-1375</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animal models Animals Antineoplastic agents Antineoplastic Agents, Alkylating - therapeutic use Apoferritins - chemistry Apoferritins - genetics Apoptosis Apoptosis - genetics Biological and medical sciences Blotting, Western Brain tumors Carmustine - therapeutic use Caspase 3 - metabolism Cations - chemistry Cell Line, Tumor Chemotherapy DNA DNA damage DNA, Neoplasm - chemistry DNA, Neoplasm - genetics DNA, Superhelical - chemistry DNA, Superhelical - genetics Dose-Response Relationship, Drug Down-Regulation Energy requirements Female Ferritin Glioma Glioma - drug therapy Glioma - genetics Glioma - pathology Glioma cells Homeostasis Humans Iron Liposomes Liposomes - chemistry Medical sciences Mice Mice, Nude Nuclei Nucleic Acid Conformation - drug effects Pharmacology. Drug treatments Plasmids RNA Interference RNA, Small Interfering - chemistry RNA, Small Interfering - genetics siRNA storage proteins Transcription Transfection Tumor cell lines Tumor cells Tumors Xenograft Model Antitumor Assays |
| title | Heavy Chain Ferritin siRNA Delivered by Cationic Liposomes Increases Sensitivity of Cancer Cells to Chemotherapeutic Agents |
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