MicroRNA-223 Enhances Radiation Sensitivity of U87MG Cells In Vitro and In Vivo by Targeting Ataxia Telangiectasia Mutated
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. Human embryonic kidney 293 T (293T) c...
Saved in:
| Published in | International journal of radiation oncology, biology, physics Vol. 88; no. 4; pp. 955 - 960 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
15.03.2014
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | 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.
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.
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).
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. |
|---|---|
| AbstractList | 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.
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.
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).
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. 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 (DER sub(2)) 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/ beta -actin mRNA 1.0 vs 1.5, P<.05). U87-223 cells were hypersensitive to radiation compared to U87-EV cells in vitro (DER sub(2) = 1.32, P<.01). Mice injected with miR-223-expressing tumors had almost the same tumors after 3 weeks (1.5 cm super(3) vs 1.7 cm super(3)). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm super(3) vs 0.829 cm super(3)). 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. 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. 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. 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 cm(3) vs 1.7 cm(3)). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm(3) vs 0.829 cm(3)). 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. 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. 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 (DER{sub 2}) 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 (DER{sub 2} = 1.32, P<.01). Mice injected with miR-223-expressing tumors had almost the same tumors after 3 weeks (1.5 cm{sup 3} vs 1.7 cm{sup 3}). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm{sup 3} vs 0.829 cm{sup 3}). 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. 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.PURPOSEAtaxia 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.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.METHODS AND MATERIALSHuman 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.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 cm(3) vs 1.7 cm(3)). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm(3) vs 0.829 cm(3)).RESULTSThe 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 cm(3) vs 1.7 cm(3)). However, irradiation significantly decreased tumor size in miR-223-expressing tumors compared to those in controls (0.033 cm(3) vs 0.829 cm(3)).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.CONCLUSIONSmiR-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. |
| Author | Wu, Xingzhong Cai, Guoxiang Zaorsky, Nicholas G. Zhu, Ji Deng, Yun Zhang, Zhen Liang, Liping Gu, Weilie Liu, Yong Liu, Fangqi Shen, Lijun |
| Author_xml | – sequence: 1 givenname: Liping surname: Liang fullname: Liang, Liping organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 2 givenname: Ji surname: Zhu fullname: Zhu, Ji organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 3 givenname: Nicholas G. surname: Zaorsky fullname: Zaorsky, Nicholas G. organization: Department of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania – sequence: 4 givenname: Yun surname: Deng fullname: Deng, Yun organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 5 givenname: Xingzhong surname: Wu fullname: Wu, Xingzhong organization: Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 6 givenname: Yong surname: Liu fullname: Liu, Yong organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 7 givenname: Fangqi surname: Liu fullname: Liu, Fangqi organization: Department of Colorectal Cancer, Fudan University, Shanghai Cancer Center, Shanghai, PR China – sequence: 8 givenname: Guoxiang surname: Cai fullname: Cai, Guoxiang organization: Department of Colorectal Cancer, Fudan University, Shanghai Cancer Center, Shanghai, PR China – sequence: 9 givenname: Weilie surname: Gu fullname: Gu, Weilie organization: Department of Colorectal Cancer, Fudan University, Shanghai Cancer Center, Shanghai, PR China – sequence: 10 givenname: Lijun surname: Shen fullname: Shen, Lijun organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China – sequence: 11 givenname: Zhen surname: Zhang fullname: Zhang, Zhen email: zhenzhang6@hotmail.com organization: Departments of Radiation Oncology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, PR China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24606854$$D View this record in MEDLINE/PubMed https://www.osti.gov/biblio/22416508$$D View this record in Osti.gov |
| BookMark | eNqVktGKEzEUhoOsuN3VNxAJeOPN1GQmycyICKXsrgtbhd0q3oVM5kw3dZrUJC0W9mF8Fp_MjK1eCLJ6FRK-_yTnfDlBR9ZZQOgpJWNKqHi5HJuld816nBNajGk-JoV4gEa0Kuus4PzTERqlE5IVCT5GJyEsCSGUluwROs6ZIKLibITuZkZ7d_1ukuV5gc_srbIaAr5WrVHROItvwAYTzdbEHXYd_lCVsws8hb4P-NJ-__bRRO-wsu1ht3W42eG58guIxi7wJKqvRuE59MouDOioQtrONlFFaB-jh53qAzw5rKdofn42n77Nrt5fXE4nV5nmdRmzsmxSi5SUQmjWkq4CKJtO1F0uaFMUvNaiFi3XHXDKgLKWFU3TNhU0eVexrjhFz_dlXYhGBm0i6FvtrE3PkXnOqOCkStSLPbX27ssGQpQrE3RqVFlwmyApZ4yQmhbkH1AiGC0rPqDPDuimWUEr196slN_JXwYSwPZA0hCCh-43QokcRMul3IuWg2hJc5m0ptirP2KprZ_Golemvy_8Zh-GNPStAT8MBZL41vhhJq0z_1tA98YarfrPsIOwdBtvk1BJZUgBeTN8xOEfDsMTdcVTgdd_L3D__T8ANcDvCg |
| CitedBy_id | crossref_primary_10_1093_carcin_bgv007 crossref_primary_10_1038_bjc_2015_60 crossref_primary_10_3892_ol_2016_5115 crossref_primary_10_1016_j_canlet_2020_10_049 crossref_primary_10_1038_s41598_018_33071_0 crossref_primary_10_1177_1073274819847226 crossref_primary_10_3892_or_2015_4196 crossref_primary_10_3390_brainsci13020350 crossref_primary_10_3390_cancers12061662 crossref_primary_10_1016_j_mrfmmm_2019_111679 crossref_primary_10_1155_2020_2727060 crossref_primary_10_3390_ijms25158191 crossref_primary_10_1016_j_lfs_2021_119798 crossref_primary_10_3389_fgene_2022_1069112 crossref_primary_10_1016_j_clon_2015_11_001 crossref_primary_10_18632_oncotarget_17600 crossref_primary_10_18632_oncotarget_1859 crossref_primary_10_1016_j_gene_2017_03_021 crossref_primary_10_1016_j_mrrev_2014_11_003 crossref_primary_10_1016_j_dnarep_2016_09_003 crossref_primary_10_1016_j_molmed_2014_07_004 |
| Cites_doi | 10.1038/ng1117 10.1371/journal.pone.0025454 10.1016/j.molcel.2010.12.005 10.1093/nar/gkn550 10.1016/j.febslet.2010.05.031 10.1016/S0360-3016(01)01489-4 10.1016/j.ijrobp.2011.05.031 10.1371/journal.pone.0011397 10.1158/1541-7786.MCR-10-0529 10.1016/j.tibs.2011.06.002 10.1016/j.febslet.2012.02.050 10.1038/sj.onc.1205485 10.1016/j.ccr.2007.09.020 10.1016/j.pharmthera.2012.10.009 10.1038/nsmb.1589 10.1371/journal.pone.0027008 10.1093/nar/gni178 10.1007/s00432-012-1154-x 10.1158/1535-7163.MCT-09-0519 |
| ContentType | Journal Article |
| Copyright | 2014 Elsevier Inc. Elsevier Inc. Copyright © 2014 Elsevier Inc. All rights reserved. |
| Copyright_xml | – notice: 2014 Elsevier Inc. – notice: Elsevier Inc. – notice: Copyright © 2014 Elsevier Inc. All rights reserved. |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 7TM OTOTI |
| DOI | 10.1016/j.ijrobp.2013.12.036 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic Nucleic Acids Abstracts OSTI.GOV |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic Nucleic Acids Abstracts |
| DatabaseTitleList | Nucleic Acids Abstracts MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1879-355X |
| EndPage | 960 |
| ExternalDocumentID | 22416508 24606854 10_1016_j_ijrobp_2013_12_036 S0360301613036985 1_s2_0_S0360301613036985 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Fudan University Radiation Medicine Research grantid: 985III-YPT06 – fundername: Shanghai Science and Technology Commission Guide grantid: 10411962800 |
| GroupedDBID | --- --K .1- .FO 0R~ 1B1 1P~ 1RT 1~5 4.4 457 4G. 53G 5RE 5VS 7-5 AAEDT AAEDW AAQFI AAQQT AAWTL AAXUO ABJNI ABLJU ABNEU ABOCM ABUDA ACGFS ACIUM ACVFH ADBBV ADCNI ADVLN AENEX AEUPX AEVXI AFPUW AFRHN AFTJW AGCQF AHHHB AIGII AITUG AJUYK AKBMS AKRWK AKYEP ALMA_UNASSIGNED_HOLDINGS AMRAJ BELOY DU5 EBS EFKBS EJD F5P FDB GBLVA HED HMO IHE J1W KOM LX3 M41 MO0 O9- OC~ OO- RNS ROL RPZ SDG SEL SES SSZ UV1 XH2 Z5R ~S- .55 .GJ 29J AALRI AAQXK ABEFU ABWVN ACRPL ADMUD ADNMO ADPAM AFCTW AFFNX AFJKZ AGRDE ASPBG AVWKF AZFZN EFJIC FEDTE FGOYB FIRID G-2 HMK HVGLF HX~ HZ~ NQ- R2- RIG SAE SEW UDS X7M XPP ZGI AAIAV AGZHU ALXNB ZA5 AAYWO AAYXX AGQPQ CITATION CGR CUY CVF ECM EIF NPM 7X8 7TM ABPTK OTOTI |
| ID | FETCH-LOGICAL-c597t-77b01310766c4d0f8ee7bf69f261b3359c696d5cfe514e14d43bbdb8eb2f84f3 |
| ISSN | 0360-3016 1879-355X |
| IngestDate | Thu May 18 22:29:48 EDT 2023 Thu Jul 10 19:07:50 EDT 2025 Tue Aug 05 11:01:36 EDT 2025 Mon Jul 21 06:01:52 EDT 2025 Thu Apr 24 23:08:05 EDT 2025 Tue Jul 01 01:49:10 EDT 2025 Fri Feb 23 02:35:54 EST 2024 Sun Feb 23 10:18:46 EST 2025 Tue Aug 26 16:37:44 EDT 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Language | English |
| License | https://www.elsevier.com/tdm/userlicense/1.0 Copyright © 2014 Elsevier Inc. All rights reserved. |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c597t-77b01310766c4d0f8ee7bf69f261b3359c696d5cfe514e14d43bbdb8eb2f84f3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| PMID | 24606854 |
| PQID | 1506417850 |
| PQPubID | 23479 |
| PageCount | 6 |
| ParticipantIDs | osti_scitechconnect_22416508 proquest_miscellaneous_1544009130 proquest_miscellaneous_1506417850 pubmed_primary_24606854 crossref_primary_10_1016_j_ijrobp_2013_12_036 crossref_citationtrail_10_1016_j_ijrobp_2013_12_036 elsevier_sciencedirect_doi_10_1016_j_ijrobp_2013_12_036 elsevier_clinicalkeyesjournals_1_s2_0_S0360301613036985 elsevier_clinicalkey_doi_10_1016_j_ijrobp_2013_12_036 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2014-03-15 |
| PublicationDateYYYYMMDD | 2014-03-15 |
| PublicationDate_xml | – month: 03 year: 2014 text: 2014-03-15 day: 15 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | International journal of radiation oncology, biology, physics |
| PublicationTitleAlternate | Int J Radiat Oncol Biol Phys |
| PublicationYear | 2014 |
| Publisher | Elsevier Inc |
| Publisher_xml | – name: Elsevier Inc |
| References | Chen, Ridzon, Broomer (bib9) 2005; 33 Jia, Li, Zhu (bib8) 2011; 6 Li, Guo, Liang (bib16) 2012; 138 Tribius, Pidel, Casper (bib3) 2001; 50 Li, Zhang, Zhang (bib15) 2011; 9 Song, Lin, Wu (bib19) 2011; 6 Wan, Mathur, Hu (bib5) 2011; 36 Yan, Ng, Zhang (bib18) 2010; 5 Golding, Rosenberg, Valerie (bib20) 2009; 8 Kinner, Wu, Staudt (bib12) 2008; 36 Wu, Li, Jia (bib14) 2012; 586 Moskwa, Buffa, Pan (bib6) 2011; 41 Derheimer, Kastan (bib1) 2010; 584 Kim, Vo, Shrivastav (bib4) 2002; 21 Rubinson, Dillon, Kwiatkowski (bib11) 2003; 33 Lal, Pan, Navarro (bib7) 2009; 16 Chen, Wang, Ng (bib17) 2011; 81 Furgason, Bahassi el (bib2) 2013; 137 Wu, Lin, Yang (bib10) 1996; 109 Fazi, Racanicchi, Zardo (bib13) 2007; 12 Kinner (10.1016/j.ijrobp.2013.12.036_bib12) 2008; 36 Tribius (10.1016/j.ijrobp.2013.12.036_bib3) 2001; 50 Jia (10.1016/j.ijrobp.2013.12.036_bib8) 2011; 6 Derheimer (10.1016/j.ijrobp.2013.12.036_bib1) 2010; 584 Rubinson (10.1016/j.ijrobp.2013.12.036_bib11) 2003; 33 Song (10.1016/j.ijrobp.2013.12.036_bib19) 2011; 6 Li (10.1016/j.ijrobp.2013.12.036_bib16) 2012; 138 Moskwa (10.1016/j.ijrobp.2013.12.036_bib6) 2011; 41 Lal (10.1016/j.ijrobp.2013.12.036_bib7) 2009; 16 Fazi (10.1016/j.ijrobp.2013.12.036_bib13) 2007; 12 Kim (10.1016/j.ijrobp.2013.12.036_bib4) 2002; 21 Li (10.1016/j.ijrobp.2013.12.036_bib15) 2011; 9 Furgason (10.1016/j.ijrobp.2013.12.036_bib2) 2013; 137 Wu (10.1016/j.ijrobp.2013.12.036_bib14) 2012; 586 Wan (10.1016/j.ijrobp.2013.12.036_bib5) 2011; 36 Golding (10.1016/j.ijrobp.2013.12.036_bib20) 2009; 8 Yan (10.1016/j.ijrobp.2013.12.036_bib18) 2010; 5 Wu (10.1016/j.ijrobp.2013.12.036_bib10) 1996; 109 Chen (10.1016/j.ijrobp.2013.12.036_bib17) 2011; 81 Chen (10.1016/j.ijrobp.2013.12.036_bib9) 2005; 33 |
| References_xml | – volume: 6 start-page: e27008 year: 2011 ident: bib8 article-title: MiR-223 suppresses cell proliferation by targeting IGF-1R publication-title: PLoS One – volume: 41 start-page: 210 year: 2011 end-page: 220 ident: bib6 article-title: miR-182-mediated downregulation of BRCA1 impacts DNA repair and sensitivity to PARP inhibitors publication-title: Mol Cell – volume: 36 start-page: 5678 year: 2008 end-page: 5694 ident: bib12 article-title: Gamma-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin publication-title: Nucleic Acids Res – volume: 6 start-page: e25454 year: 2011 ident: bib19 article-title: miR-18a impairs DNA damage response through downregulation of ataxia telangiectasia mutated (ATM) kinase publication-title: PLoS One – volume: 21 start-page: 3864 year: 2002 end-page: 3871 ident: bib4 article-title: Aberrant methylation of the ATM promoter correlates with increased radiosensitivity in a human colorectal tumor cell line publication-title: Oncogene – volume: 36 start-page: 478 year: 2011 end-page: 484 ident: bib5 article-title: miRNA response to DNA damage publication-title: Trends Biochem Sci – volume: 33 start-page: 401 year: 2003 end-page: 406 ident: bib11 article-title: A lentivirus-based system to functionally silence genes in primary mammalian cells, stem cells and transgenic mice by RNA interference publication-title: Nat Genet – volume: 81 start-page: 1524 year: 2011 end-page: 1529 ident: bib17 article-title: Radiosensitizing effects of ectopic miR-101 on non-small-cell lung cancer cells depend on the endogenous miR-101 level publication-title: Int J Radiat Oncol Biol Phys – volume: 12 start-page: 457 year: 2007 end-page: 466 ident: bib13 article-title: Epigenetic silencing of the myelopoiesis regulator microRNA-223 by the AML1/ETO oncoprotein publication-title: Cancer Cell – volume: 33 start-page: e179 year: 2005 ident: bib9 article-title: Real-time quantification of microRNAs by stem-loop RT-PCR publication-title: Nucleic Acids Res – volume: 9 start-page: 824 year: 2011 end-page: 833 ident: bib15 article-title: miRNA-223 promotes gastric cancer invasion and metastasis by targeting tumor suppressor EPB41L3 publication-title: Mol Cancer Res – volume: 586 start-page: 1038 year: 2012 end-page: 1043 ident: bib14 article-title: MicroRNA-223 regulates FOXO1 expression and cell proliferation publication-title: FEBS Lett – volume: 584 start-page: 3675 year: 2010 end-page: 3681 ident: bib1 article-title: Multiple roles of ATM in monitoring and maintaining DNA integrity publication-title: FEBS Lett – volume: 5 start-page: e11397 year: 2010 ident: bib18 article-title: Targeting DNA-PKcs and ATM with miR-101 sensitizes tumors to radiation publication-title: PLoS One – volume: 8 start-page: 2894 year: 2009 end-page: 2902 ident: bib20 article-title: Improved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises insulin, AKT and ERK prosurvival signaling, and inhibits migration and invasion publication-title: Mol Cancer Ther – volume: 16 start-page: 492 year: 2009 end-page: 498 ident: bib7 article-title: miR-24-mediated downregulation of H2AX suppresses DNA repair in terminally differentiated blood cells publication-title: Nat Struct Mol Biol – volume: 137 start-page: 298 year: 2013 end-page: 308 ident: bib2 article-title: Targeting DNA repair mechanisms in cancer publication-title: Pharmacol Ther – volume: 109 start-page: 295 year: 1996 end-page: 299 ident: bib10 article-title: Detection of PML-RAR alpha in patients with APL during follow-up period publication-title: Chin Med J (Engl) – volume: 138 start-page: 763 year: 2012 end-page: 774 ident: bib16 article-title: MicroRNA-223 functions as an oncogene in human gastric cancer by targeting FBXW7/hCdc4 publication-title: J Cancer Res Clin Oncol – volume: 50 start-page: 511 year: 2001 end-page: 523 ident: bib3 article-title: ATM protein expression correlates with radioresistance in primary glioblastoma cells in culture publication-title: Int J Radiat Oncol Biol Phys – volume: 33 start-page: 401 year: 2003 ident: 10.1016/j.ijrobp.2013.12.036_bib11 article-title: A lentivirus-based system to functionally silence genes in primary mammalian cells, stem cells and transgenic mice by RNA interference publication-title: Nat Genet doi: 10.1038/ng1117 – volume: 6 start-page: e25454 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib19 article-title: miR-18a impairs DNA damage response through downregulation of ataxia telangiectasia mutated (ATM) kinase publication-title: PLoS One doi: 10.1371/journal.pone.0025454 – volume: 41 start-page: 210 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib6 article-title: miR-182-mediated downregulation of BRCA1 impacts DNA repair and sensitivity to PARP inhibitors publication-title: Mol Cell doi: 10.1016/j.molcel.2010.12.005 – volume: 36 start-page: 5678 year: 2008 ident: 10.1016/j.ijrobp.2013.12.036_bib12 article-title: Gamma-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin publication-title: Nucleic Acids Res doi: 10.1093/nar/gkn550 – volume: 584 start-page: 3675 year: 2010 ident: 10.1016/j.ijrobp.2013.12.036_bib1 article-title: Multiple roles of ATM in monitoring and maintaining DNA integrity publication-title: FEBS Lett doi: 10.1016/j.febslet.2010.05.031 – volume: 50 start-page: 511 year: 2001 ident: 10.1016/j.ijrobp.2013.12.036_bib3 article-title: ATM protein expression correlates with radioresistance in primary glioblastoma cells in culture publication-title: Int J Radiat Oncol Biol Phys doi: 10.1016/S0360-3016(01)01489-4 – volume: 81 start-page: 1524 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib17 article-title: Radiosensitizing effects of ectopic miR-101 on non-small-cell lung cancer cells depend on the endogenous miR-101 level publication-title: Int J Radiat Oncol Biol Phys doi: 10.1016/j.ijrobp.2011.05.031 – volume: 5 start-page: e11397 year: 2010 ident: 10.1016/j.ijrobp.2013.12.036_bib18 article-title: Targeting DNA-PKcs and ATM with miR-101 sensitizes tumors to radiation publication-title: PLoS One doi: 10.1371/journal.pone.0011397 – volume: 9 start-page: 824 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib15 article-title: miRNA-223 promotes gastric cancer invasion and metastasis by targeting tumor suppressor EPB41L3 publication-title: Mol Cancer Res doi: 10.1158/1541-7786.MCR-10-0529 – volume: 36 start-page: 478 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib5 article-title: miRNA response to DNA damage publication-title: Trends Biochem Sci doi: 10.1016/j.tibs.2011.06.002 – volume: 586 start-page: 1038 year: 2012 ident: 10.1016/j.ijrobp.2013.12.036_bib14 article-title: MicroRNA-223 regulates FOXO1 expression and cell proliferation publication-title: FEBS Lett doi: 10.1016/j.febslet.2012.02.050 – volume: 21 start-page: 3864 year: 2002 ident: 10.1016/j.ijrobp.2013.12.036_bib4 article-title: Aberrant methylation of the ATM promoter correlates with increased radiosensitivity in a human colorectal tumor cell line publication-title: Oncogene doi: 10.1038/sj.onc.1205485 – volume: 12 start-page: 457 year: 2007 ident: 10.1016/j.ijrobp.2013.12.036_bib13 article-title: Epigenetic silencing of the myelopoiesis regulator microRNA-223 by the AML1/ETO oncoprotein publication-title: Cancer Cell doi: 10.1016/j.ccr.2007.09.020 – volume: 137 start-page: 298 year: 2013 ident: 10.1016/j.ijrobp.2013.12.036_bib2 article-title: Targeting DNA repair mechanisms in cancer publication-title: Pharmacol Ther doi: 10.1016/j.pharmthera.2012.10.009 – volume: 16 start-page: 492 year: 2009 ident: 10.1016/j.ijrobp.2013.12.036_bib7 article-title: miR-24-mediated downregulation of H2AX suppresses DNA repair in terminally differentiated blood cells publication-title: Nat Struct Mol Biol doi: 10.1038/nsmb.1589 – volume: 6 start-page: e27008 year: 2011 ident: 10.1016/j.ijrobp.2013.12.036_bib8 article-title: MiR-223 suppresses cell proliferation by targeting IGF-1R publication-title: PLoS One doi: 10.1371/journal.pone.0027008 – volume: 33 start-page: e179 year: 2005 ident: 10.1016/j.ijrobp.2013.12.036_bib9 article-title: Real-time quantification of microRNAs by stem-loop RT-PCR publication-title: Nucleic Acids Res doi: 10.1093/nar/gni178 – volume: 109 start-page: 295 year: 1996 ident: 10.1016/j.ijrobp.2013.12.036_bib10 article-title: Detection of PML-RAR alpha in patients with APL during follow-up period publication-title: Chin Med J (Engl) – volume: 138 start-page: 763 year: 2012 ident: 10.1016/j.ijrobp.2013.12.036_bib16 article-title: MicroRNA-223 functions as an oncogene in human gastric cancer by targeting FBXW7/hCdc4 publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-012-1154-x – volume: 8 start-page: 2894 year: 2009 ident: 10.1016/j.ijrobp.2013.12.036_bib20 article-title: Improved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises insulin, AKT and ERK prosurvival signaling, and inhibits migration and invasion publication-title: Mol Cancer Ther doi: 10.1158/1535-7163.MCT-09-0519 |
| SSID | ssj0001174 |
| Score | 2.2568424 |
| Snippet | Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined the... Purpose Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We examined... Purpose: Ataxia telangiectasia mutated (ATM) protein is important in the DNA damage response because it repairs radiation-induced damage in cancers. We... |
| SourceID | osti proquest pubmed crossref elsevier |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 955 |
| SubjectTerms | 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 |
| URI | https://www.clinicalkey.com/#!/content/1-s2.0-S0360301613036985 https://www.clinicalkey.es/playcontent/1-s2.0-S0360301613036985 https://dx.doi.org/10.1016/j.ijrobp.2013.12.036 https://www.ncbi.nlm.nih.gov/pubmed/24606854 https://www.proquest.com/docview/1506417850 https://www.proquest.com/docview/1544009130 https://www.osti.gov/biblio/22416508 |
| Volume | 88 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3NbtNAEF6FVEJcEP8EClokeooc-Wf9d4yi0kJJDyGFcLK89hoSRTZKnAgQD8Oz8Ag8ETO7a8chLS29RMnKa288n2e-Gc_MEvISPH8nyeLUsHkSGEykzIiFmxmpxxOf8ZgF8o3u8NQ7PmNvJu6k1frdyFpalbyXfD-3ruQ6UoUxkCtWyf6HZOuTwgB8B_nCJ0gYPq8k4yFm041O-wZY3-5h_hkluOyOsN2AVgQ5pmStddrFWeAPj7oDMZ8vQS8cDOyDvvl-Wi4KnRRcjawLJKVjmSMuoyZl_HUad8cCg5tT0JBYedkdrpCnbu3zuR1ebDSlWNRLKvKkro_hm1IZFWCp-f3bqQ5jy621P22i2yuJumk9EBcLHf0FSKObvuwe9WpyLtRJPq7yZnDDYpjdpco7VcStqrrZSgoFowu2w7R0C22luAM_NIA7TZqaPQgaCGYNNR2q1sDa4odqR4MdY6LiGrPedLYoOPY2tRwZOnb-6t0t2cA7XBUuSpKCMHBvkD0bXBe7Tfb6J6MPJzU_sHRv8OpfVAWdMutw91oXEaZ2ATbgYr9I8qPxHXJbOza0r1B6l7REfo_cHOrUjfvkRxOstAIrrcFKG2ClRUYlWKkEK32d__opgUoBqPrXuqD8G61BShVI6TZIqQbpAzJ-dTgeHBt66w8jAQ-3BJ8P4_OW6XtewlIzC4TweeaFGTj83HHcMPFCL3WTTADhFxZLmcN5ygPB7SxgmfOQtPMiF48JdSwbWyK6dpYxFpopB3UUx7bPvNA3szTuEKe6vVGi2-Lj7izzqMp_nEVKKBEKJbLsCITSIUY964tqC3PJ8W4luagqeQYjHQHULpnnnzdPLPUjvIysaAlHRjvwa87UZFqR5Ctccx-hhbOwj3SCCXcwDbk-unMd8qKCXASmCN8vxrkoVrAUbH5p-YFr_usYBqwhhFV2yCOF1_oG2swzvcBlT6699Kfk1kaL7JN2uViJZ-A0lPy5fgr_ADT4GBY |
| linkProvider | Library Specific Holdings |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=MicroRNA-223+Enhances+Radiation+Sensitivity+of+U87MG+Cells+In%C2%A0Vitro+and+In%C2%A0Vivo+by+Targeting+Ataxia+Telangiectasia+Mutated&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.au=Liang%2C+Liping&rft.au=Zhu%2C+Ji&rft.au=Zaorsky%2C+Nicholas+G.&rft.au=Deng%2C+Yun&rft.date=2014-03-15&rft.pub=Elsevier+Inc&rft.issn=0360-3016&rft.eissn=1879-355X&rft.volume=88&rft.issue=4&rft.spage=955&rft.epage=960&rft_id=info:doi/10.1016%2Fj.ijrobp.2013.12.036&rft.externalDocID=S0360301613036985 |
| thumbnail_m | http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=https%3A%2F%2Fcdn.clinicalkey.com%2Fck-thumbnails%2F03603016%2FS0360301614X00039%2Fcov150h.gif |