MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated
Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the effect of microRNA-223 (miR-223), a regulator of ATM expression, on radiation sensitivity of cancer cells. Methods and Materials Human e...
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| Veröffentlicht in: | International journal of radiation oncology, biology, physics biology, physics, 2014-03, Vol.88 (4), p.955-960 |
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| creator | Liang, Liping, MD Zhu, Ji, MD, PhD Zaorsky, Nicholas G., MD Deng, Yun, MD Wu, Xingzhong, PhD Liu, Yong, PhD Liu, Fangqi, MD Cai, Guoxiang, MD, PhD Gu, Weilie, MD Shen, Lijun, MD Zhang, Zhen, MD, PhD |
| description | Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the effect of microRNA-223 (miR-223), a regulator of ATM expression, on radiation sensitivity of cancer cells. Methods and Materials Human embryonic kidney 293 T (293T) cells were infected with pLL3.7-miR-223 plasmid to generate the pLL3.7-miR-223 and -empty virus (EV) lentivirus (miR-223 and EV). A dual luciferase assay in which the reporter contained wild-type 3′ untranslated region (UTR) of ATM was performed. U87MG cells were infected with miR-223 or EV to establish the overexpressed stable cell lines (U87-223 or U87-EV, respectively). Cells were irradiated in vitro, and dose enhancement ratios at 2 Gy (DER2 ) were calculated. Hind legs of BALB/c athymic mice were injected with U87-223 or U87-EV cells; after 2 weeks, half of the tumors were irradiated. Tumor volumes were tracked for a total of 5 weeks. Results The dual luciferase reporter assay showed a significant reduction in luciferase activity of 293T cells cotransfected with miR-223 and the ATM 3′UTR compared to that in EV control. Overexpression of miR-223 in U87MG cells showed that ATM expression was significantly downregulated in the U87-223 cells compared to that in U87-EV (ATM/β-actin mRNA 1.0 vs 1.5, P |
| doi_str_mv | 10.1016/j.ijrobp.2013.12.036 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_osti_</sourceid><recordid>TN_cdi_osti_scitechconnect_22416508</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0360301613036985</els_id><sourcerecordid>1506417850</sourcerecordid><originalsourceid>FETCH-LOGICAL-c544t-9377cbe1142bf4fec1d8497a5f3eb42fe482d908fb643eed804c00b513f5545e3</originalsourceid><addsrcrecordid>eNqNkstuEzEUhkcIREPhDRCyxIbNDL7OZYMURaVUakBqU8TO8njOpA4TO7U9EZF4GJ6FJ8OjBBZsYGUd6zuX__wny14SXBBMyrebwmy8a3cFxYQVhBaYlY-yGamrJmdCfHmczdIPzlmCz7JnIWwwxoRU_Gl2RnmJy1rwWfZ9abR3Nx_nOaUMXdh7ZTUEdKM6o6JxFt2CDSaavYkH5Hp0V1fLS7SAYQjoyv788dlE75Cy3SnaO9Qe0Er5NURj12ge1Tej0AoGZdcGdFQhhcsxqgjd8-xJr4YAL07veXb3_mK1-JBff7q8Wsyvcy04j3nDqkq3QAinbc970KSreVMp0TNoOe2B17RrcN23JWcAXY25xrgVhPVCcAHsPHt9rOtCNDJoE0Hfa2dtmkdSykkpcJ2oN0dq593DCCHKrQk6KVUW3BgkScNg3BCG_wPFJSdVLSaUH9G05hA89HLnzVb5gyRYTkbKjTwaKScjJaEy2ZbSXp06jO0Wuj9Jv51LwLsjAGlxewN-0gXJvM74SVbnzL86_F1AD8YarYavcICwcaO3yRRJZEgJ8nY6pumWJv1lUwv2CzC3xUw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1506417850</pqid></control><display><type>article</type><title>MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Liang, Liping, MD ; Zhu, Ji, MD, PhD ; Zaorsky, Nicholas G., MD ; Deng, Yun, MD ; Wu, Xingzhong, PhD ; Liu, Yong, PhD ; Liu, Fangqi, MD ; Cai, Guoxiang, MD, PhD ; Gu, Weilie, MD ; Shen, Lijun, MD ; Zhang, Zhen, MD, PhD</creator><creatorcontrib>Liang, Liping, MD ; Zhu, Ji, MD, PhD ; Zaorsky, Nicholas G., MD ; Deng, Yun, MD ; Wu, Xingzhong, PhD ; Liu, Yong, PhD ; Liu, Fangqi, MD ; Cai, Guoxiang, MD, PhD ; Gu, Weilie, MD ; Shen, Lijun, MD ; Zhang, Zhen, MD, PhD</creatorcontrib><description>Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the effect of microRNA-223 (miR-223), a regulator of ATM expression, on radiation sensitivity of cancer cells. Methods and Materials Human embryonic kidney 293 T (293T) cells were infected with pLL3.7-miR-223 plasmid to generate the pLL3.7-miR-223 and -empty virus (EV) lentivirus (miR-223 and EV). A dual luciferase assay in which the reporter contained wild-type 3′ untranslated region (UTR) of ATM was performed. U87MG cells were infected with miR-223 or EV to establish the overexpressed stable cell lines (U87-223 or U87-EV, respectively). Cells were irradiated in vitro, and dose enhancement ratios at 2 Gy (DER2 ) were calculated. Hind legs of BALB/c athymic mice were injected with U87-223 or U87-EV cells; after 2 weeks, half of the tumors were irradiated. Tumor volumes were tracked for a total of 5 weeks. Results The dual luciferase reporter assay showed a significant reduction in luciferase activity of 293T cells cotransfected with miR-223 and the ATM 3′UTR compared to that in EV control. Overexpression of miR-223 in U87MG cells showed that ATM expression was significantly downregulated in the U87-223 cells compared to that in U87-EV (ATM/β-actin mRNA 1.0 vs 1.5, P <.05). U87-223 cells were hypersensitive to radiation compared to U87-EV cells in vitro (DER2 = 1.32, P <.01). Mice injected with miR-223-expressing tumors had almost the same tumors after 3 weeks (1.5 cm3 vs 1.7 cm3 ). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm3 vs 0.829 cm3 ). Conclusions miR-223 overexpression downregulates ATM expression and sensitizes U87 cells to radiation in vitro and in vivo. MicroRNA-223 may be a novel cancer-targeting therapy, although its cancer- and patient-specific roles are currently undefined.</description><identifier>ISSN: 0360-3016</identifier><identifier>EISSN: 1879-355X</identifier><identifier>DOI: 10.1016/j.ijrobp.2013.12.036</identifier><identifier>PMID: 24606854</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>ACTIN ; Animals ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Cell Line, Tumor ; COMPARATIVE EVALUATIONS ; DNA DAMAGES ; Down Syndrome ; Genes, Reporter ; Hematology, Oncology and Palliative Medicine ; Heterografts ; Humans ; IN VITRO ; IN VIVO ; IRRADIATION ; KIDNEYS ; Lentivirus ; LUCIFERASE ; Luciferases - metabolism ; MESSENGER-RNA ; MICE ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - physiology ; NEOPLASMS ; PATIENTS ; Radiation Tolerance - physiology ; Radiology ; RADIOLOGY AND NUCLEAR MEDICINE ; RADIOSENSITIVITY ; VIRUSES</subject><ispartof>International journal of radiation oncology, biology, physics, 2014-03, Vol.88 (4), p.955-960</ispartof><rights>Elsevier Inc.</rights><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-9377cbe1142bf4fec1d8497a5f3eb42fe482d908fb643eed804c00b513f5545e3</citedby><cites>FETCH-LOGICAL-c544t-9377cbe1142bf4fec1d8497a5f3eb42fe482d908fb643eed804c00b513f5545e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijrobp.2013.12.036$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24606854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22416508$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, Liping, MD</creatorcontrib><creatorcontrib>Zhu, Ji, MD, PhD</creatorcontrib><creatorcontrib>Zaorsky, Nicholas G., MD</creatorcontrib><creatorcontrib>Deng, Yun, MD</creatorcontrib><creatorcontrib>Wu, Xingzhong, PhD</creatorcontrib><creatorcontrib>Liu, Yong, PhD</creatorcontrib><creatorcontrib>Liu, Fangqi, MD</creatorcontrib><creatorcontrib>Cai, Guoxiang, MD, PhD</creatorcontrib><creatorcontrib>Gu, Weilie, MD</creatorcontrib><creatorcontrib>Shen, Lijun, MD</creatorcontrib><creatorcontrib>Zhang, Zhen, MD, PhD</creatorcontrib><title>MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated</title><title>International journal of radiation oncology, biology, physics</title><addtitle>Int J Radiat Oncol Biol Phys</addtitle><description>Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the effect of microRNA-223 (miR-223), a regulator of ATM expression, on radiation sensitivity of cancer cells. Methods and Materials Human embryonic kidney 293 T (293T) cells were infected with pLL3.7-miR-223 plasmid to generate the pLL3.7-miR-223 and -empty virus (EV) lentivirus (miR-223 and EV). A dual luciferase assay in which the reporter contained wild-type 3′ untranslated region (UTR) of ATM was performed. U87MG cells were infected with miR-223 or EV to establish the overexpressed stable cell lines (U87-223 or U87-EV, respectively). Cells were irradiated in vitro, and dose enhancement ratios at 2 Gy (DER2 ) were calculated. Hind legs of BALB/c athymic mice were injected with U87-223 or U87-EV cells; after 2 weeks, half of the tumors were irradiated. Tumor volumes were tracked for a total of 5 weeks. Results The dual luciferase reporter assay showed a significant reduction in luciferase activity of 293T cells cotransfected with miR-223 and the ATM 3′UTR compared to that in EV control. Overexpression of miR-223 in U87MG cells showed that ATM expression was significantly downregulated in the U87-223 cells compared to that in U87-EV (ATM/β-actin mRNA 1.0 vs 1.5, P <.05). U87-223 cells were hypersensitive to radiation compared to U87-EV cells in vitro (DER2 = 1.32, P <.01). Mice injected with miR-223-expressing tumors had almost the same tumors after 3 weeks (1.5 cm3 vs 1.7 cm3 ). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm3 vs 0.829 cm3 ). Conclusions miR-223 overexpression downregulates ATM expression and sensitizes U87 cells to radiation in vitro and in vivo. MicroRNA-223 may be a novel cancer-targeting therapy, although its cancer- and patient-specific roles are currently undefined.</description><subject>ACTIN</subject><subject>Animals</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>COMPARATIVE EVALUATIONS</subject><subject>DNA DAMAGES</subject><subject>Down Syndrome</subject><subject>Genes, Reporter</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Heterografts</subject><subject>Humans</subject><subject>IN VITRO</subject><subject>IN VIVO</subject><subject>IRRADIATION</subject><subject>KIDNEYS</subject><subject>Lentivirus</subject><subject>LUCIFERASE</subject><subject>Luciferases - metabolism</subject><subject>MESSENGER-RNA</subject><subject>MICE</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNAs - physiology</subject><subject>NEOPLASMS</subject><subject>PATIENTS</subject><subject>Radiation Tolerance - physiology</subject><subject>Radiology</subject><subject>RADIOLOGY AND NUCLEAR MEDICINE</subject><subject>RADIOSENSITIVITY</subject><subject>VIRUSES</subject><issn>0360-3016</issn><issn>1879-355X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkstuEzEUhkcIREPhDRCyxIbNDL7OZYMURaVUakBqU8TO8njOpA4TO7U9EZF4GJ6FJ8OjBBZsYGUd6zuX__wny14SXBBMyrebwmy8a3cFxYQVhBaYlY-yGamrJmdCfHmczdIPzlmCz7JnIWwwxoRU_Gl2RnmJy1rwWfZ9abR3Nx_nOaUMXdh7ZTUEdKM6o6JxFt2CDSaavYkH5Hp0V1fLS7SAYQjoyv788dlE75Cy3SnaO9Qe0Er5NURj12ge1Tej0AoGZdcGdFQhhcsxqgjd8-xJr4YAL07veXb3_mK1-JBff7q8Wsyvcy04j3nDqkq3QAinbc970KSreVMp0TNoOe2B17RrcN23JWcAXY25xrgVhPVCcAHsPHt9rOtCNDJoE0Hfa2dtmkdSykkpcJ2oN0dq593DCCHKrQk6KVUW3BgkScNg3BCG_wPFJSdVLSaUH9G05hA89HLnzVb5gyRYTkbKjTwaKScjJaEy2ZbSXp06jO0Wuj9Jv51LwLsjAGlxewN-0gXJvM74SVbnzL86_F1AD8YarYavcICwcaO3yRRJZEgJ8nY6pumWJv1lUwv2CzC3xUw</recordid><startdate>20140315</startdate><enddate>20140315</enddate><creator>Liang, Liping, MD</creator><creator>Zhu, Ji, MD, PhD</creator><creator>Zaorsky, Nicholas G., MD</creator><creator>Deng, Yun, MD</creator><creator>Wu, Xingzhong, PhD</creator><creator>Liu, Yong, PhD</creator><creator>Liu, Fangqi, MD</creator><creator>Cai, Guoxiang, MD, PhD</creator><creator>Gu, Weilie, MD</creator><creator>Shen, Lijun, MD</creator><creator>Zhang, Zhen, MD, PhD</creator><general>Elsevier Inc</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>7X8</scope><scope>7TM</scope><scope>OTOTI</scope></search><sort><creationdate>20140315</creationdate><title>MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated</title><author>Liang, Liping, MD ; Zhu, Ji, MD, PhD ; Zaorsky, Nicholas G., MD ; Deng, Yun, MD ; Wu, Xingzhong, PhD ; Liu, Yong, PhD ; Liu, Fangqi, MD ; Cai, Guoxiang, MD, PhD ; Gu, Weilie, MD ; Shen, Lijun, MD ; Zhang, Zhen, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-9377cbe1142bf4fec1d8497a5f3eb42fe482d908fb643eed804c00b513f5545e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>ACTIN</topic><topic>Animals</topic><topic>Ataxia Telangiectasia Mutated Proteins - metabolism</topic><topic>Cell Line, Tumor</topic><topic>COMPARATIVE EVALUATIONS</topic><topic>DNA DAMAGES</topic><topic>Down Syndrome</topic><topic>Genes, Reporter</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Heterografts</topic><topic>Humans</topic><topic>IN VITRO</topic><topic>IN VIVO</topic><topic>IRRADIATION</topic><topic>KIDNEYS</topic><topic>Lentivirus</topic><topic>LUCIFERASE</topic><topic>Luciferases - metabolism</topic><topic>MESSENGER-RNA</topic><topic>MICE</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNAs - physiology</topic><topic>NEOPLASMS</topic><topic>PATIENTS</topic><topic>Radiation Tolerance - physiology</topic><topic>Radiology</topic><topic>RADIOLOGY AND NUCLEAR MEDICINE</topic><topic>RADIOSENSITIVITY</topic><topic>VIRUSES</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liang, Liping, MD</creatorcontrib><creatorcontrib>Zhu, Ji, MD, PhD</creatorcontrib><creatorcontrib>Zaorsky, Nicholas G., MD</creatorcontrib><creatorcontrib>Deng, Yun, MD</creatorcontrib><creatorcontrib>Wu, Xingzhong, PhD</creatorcontrib><creatorcontrib>Liu, Yong, PhD</creatorcontrib><creatorcontrib>Liu, Fangqi, MD</creatorcontrib><creatorcontrib>Cai, Guoxiang, MD, PhD</creatorcontrib><creatorcontrib>Gu, Weilie, MD</creatorcontrib><creatorcontrib>Shen, Lijun, MD</creatorcontrib><creatorcontrib>Zhang, Zhen, MD, PhD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><collection>OSTI.GOV</collection><jtitle>International journal of radiation oncology, biology, physics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, Liping, MD</au><au>Zhu, Ji, MD, PhD</au><au>Zaorsky, Nicholas G., MD</au><au>Deng, Yun, MD</au><au>Wu, Xingzhong, PhD</au><au>Liu, Yong, PhD</au><au>Liu, Fangqi, MD</au><au>Cai, Guoxiang, MD, PhD</au><au>Gu, Weilie, MD</au><au>Shen, Lijun, MD</au><au>Zhang, Zhen, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated</atitle><jtitle>International journal of radiation oncology, biology, physics</jtitle><addtitle>Int J Radiat Oncol Biol Phys</addtitle><date>2014-03-15</date><risdate>2014</risdate><volume>88</volume><issue>4</issue><spage>955</spage><epage>960</epage><pages>955-960</pages><issn>0360-3016</issn><eissn>1879-355X</eissn><abstract>Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the effect of microRNA-223 (miR-223), a regulator of ATM expression, on radiation sensitivity of cancer cells. Methods and Materials Human embryonic kidney 293 T (293T) cells were infected with pLL3.7-miR-223 plasmid to generate the pLL3.7-miR-223 and -empty virus (EV) lentivirus (miR-223 and EV). A dual luciferase assay in which the reporter contained wild-type 3′ untranslated region (UTR) of ATM was performed. U87MG cells were infected with miR-223 or EV to establish the overexpressed stable cell lines (U87-223 or U87-EV, respectively). Cells were irradiated in vitro, and dose enhancement ratios at 2 Gy (DER2 ) were calculated. Hind legs of BALB/c athymic mice were injected with U87-223 or U87-EV cells; after 2 weeks, half of the tumors were irradiated. Tumor volumes were tracked for a total of 5 weeks. Results The dual luciferase reporter assay showed a significant reduction in luciferase activity of 293T cells cotransfected with miR-223 and the ATM 3′UTR compared to that in EV control. Overexpression of miR-223 in U87MG cells showed that ATM expression was significantly downregulated in the U87-223 cells compared to that in U87-EV (ATM/β-actin mRNA 1.0 vs 1.5, P <.05). U87-223 cells were hypersensitive to radiation compared to U87-EV cells in vitro (DER2 = 1.32, P <.01). Mice injected with miR-223-expressing tumors had almost the same tumors after 3 weeks (1.5 cm3 vs 1.7 cm3 ). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm3 vs 0.829 cm3 ). Conclusions miR-223 overexpression downregulates ATM expression and sensitizes U87 cells to radiation in vitro and in vivo. MicroRNA-223 may be a novel cancer-targeting therapy, although its cancer- and patient-specific roles are currently undefined.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24606854</pmid><doi>10.1016/j.ijrobp.2013.12.036</doi><tpages>6</tpages></addata></record> |
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| subjects | ACTIN Animals Ataxia Telangiectasia Mutated Proteins - metabolism Cell Line, Tumor COMPARATIVE EVALUATIONS DNA DAMAGES Down Syndrome Genes, Reporter Hematology, Oncology and Palliative Medicine Heterografts Humans IN VITRO IN VIVO IRRADIATION KIDNEYS Lentivirus LUCIFERASE Luciferases - metabolism MESSENGER-RNA MICE Mice, Inbred BALB C Mice, Nude MicroRNAs - physiology NEOPLASMS PATIENTS Radiation Tolerance - physiology Radiology RADIOLOGY AND NUCLEAR MEDICINE RADIOSENSITIVITY VIRUSES |
| title | MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated |
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