MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell
Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic ce...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kim, Jae-Sung [verfasserIn] Park, Sun-Young [verfasserIn] Lee, Seul Ah [verfasserIn] Park, Min-Gyeong [verfasserIn] Yu, Sun-Kyoung [verfasserIn] Lee, Myoung-Hwa [verfasserIn] Park, Mi-Ra [verfasserIn] Kim, Su-Gwan [verfasserIn] Oh, Ji-Su [verfasserIn] Lee, Sook-Young [verfasserIn] Kim, Chun Sung [verfasserIn] Kim, Heung-Joong [verfasserIn] Chun, Hong Sung [verfasserIn] Kim, Jin-Soo [verfasserIn] Moon, Sung-Min [verfasserIn] Kim, Do Kyung [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Molecular and cellular biochemistry - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973, 387(2013), 1-2 vom: 29. Okt., Seite 71-79 |
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| Übergeordnetes Werk: |
volume:387 ; year:2013 ; number:1-2 ; day:29 ; month:10 ; pages:71-79 |
| Links: |
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| DOI / URN: |
10.1007/s11010-013-1872-7 |
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| Katalog-ID: |
SPR015643190 |
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| 100 | 1 | |a Kim, Jae-Sung |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
| 264 | 1 | |c 2013 | |
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| 520 | |a Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. | ||
| 650 | 4 | |a MicroRNA (miRNA) |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a AXIN-2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Oral carcinoma |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Oncogenic activity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Apoptosis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Park, Sun-Young |e verfasserin |4 aut | |
| 700 | 1 | |a Lee, Seul Ah |e verfasserin |4 aut | |
| 700 | 1 | |a Park, Min-Gyeong |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Sun-Kyoung |e verfasserin |4 aut | |
| 700 | 1 | |a Lee, Myoung-Hwa |e verfasserin |4 aut | |
| 700 | 1 | |a Park, Mi-Ra |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Su-Gwan |e verfasserin |4 aut | |
| 700 | 1 | |a Oh, Ji-Su |e verfasserin |4 aut | |
| 700 | 1 | |a Lee, Sook-Young |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Chun Sung |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Heung-Joong |e verfasserin |4 aut | |
| 700 | 1 | |a Chun, Hong Sung |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Jin-Soo |e verfasserin |4 aut | |
| 700 | 1 | |a Moon, Sung-Min |e verfasserin |4 aut | |
| 700 | 1 | |a Kim, Do Kyung |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Molecular and cellular biochemistry |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 |g 387(2013), 1-2 vom: 29. Okt., Seite 71-79 |w (DE-627)32042975X |w (DE-600)2003615-2 |x 1573-4919 |7 nnns |
| 773 | 1 | 8 | |g volume:387 |g year:2013 |g number:1-2 |g day:29 |g month:10 |g pages:71-79 |
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10.1007/s11010-013-1872-7 doi (DE-627)SPR015643190 (SPR)s11010-013-1872-7-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Kim, Jae-Sung verfasserin aut MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Park, Sun-Young verfasserin aut Lee, Seul Ah verfasserin aut Park, Min-Gyeong verfasserin aut Yu, Sun-Kyoung verfasserin aut Lee, Myoung-Hwa verfasserin aut Park, Mi-Ra verfasserin aut Kim, Su-Gwan verfasserin aut Oh, Ji-Su verfasserin aut Lee, Sook-Young verfasserin aut Kim, Chun Sung verfasserin aut Kim, Heung-Joong verfasserin aut Chun, Hong Sung verfasserin aut Kim, Jin-Soo verfasserin aut Moon, Sung-Min verfasserin aut Kim, Do Kyung verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 387(2013), 1-2 vom: 29. Okt., Seite 71-79 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 https://dx.doi.org/10.1007/s11010-013-1872-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 387 2013 1-2 29 10 71-79 |
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10.1007/s11010-013-1872-7 doi (DE-627)SPR015643190 (SPR)s11010-013-1872-7-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Kim, Jae-Sung verfasserin aut MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Park, Sun-Young verfasserin aut Lee, Seul Ah verfasserin aut Park, Min-Gyeong verfasserin aut Yu, Sun-Kyoung verfasserin aut Lee, Myoung-Hwa verfasserin aut Park, Mi-Ra verfasserin aut Kim, Su-Gwan verfasserin aut Oh, Ji-Su verfasserin aut Lee, Sook-Young verfasserin aut Kim, Chun Sung verfasserin aut Kim, Heung-Joong verfasserin aut Chun, Hong Sung verfasserin aut Kim, Jin-Soo verfasserin aut Moon, Sung-Min verfasserin aut Kim, Do Kyung verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 387(2013), 1-2 vom: 29. Okt., Seite 71-79 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 https://dx.doi.org/10.1007/s11010-013-1872-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 387 2013 1-2 29 10 71-79 |
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10.1007/s11010-013-1872-7 doi (DE-627)SPR015643190 (SPR)s11010-013-1872-7-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Kim, Jae-Sung verfasserin aut MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Park, Sun-Young verfasserin aut Lee, Seul Ah verfasserin aut Park, Min-Gyeong verfasserin aut Yu, Sun-Kyoung verfasserin aut Lee, Myoung-Hwa verfasserin aut Park, Mi-Ra verfasserin aut Kim, Su-Gwan verfasserin aut Oh, Ji-Su verfasserin aut Lee, Sook-Young verfasserin aut Kim, Chun Sung verfasserin aut Kim, Heung-Joong verfasserin aut Chun, Hong Sung verfasserin aut Kim, Jin-Soo verfasserin aut Moon, Sung-Min verfasserin aut Kim, Do Kyung verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 387(2013), 1-2 vom: 29. Okt., Seite 71-79 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 https://dx.doi.org/10.1007/s11010-013-1872-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 387 2013 1-2 29 10 71-79 |
| allfieldsGer |
10.1007/s11010-013-1872-7 doi (DE-627)SPR015643190 (SPR)s11010-013-1872-7-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Kim, Jae-Sung verfasserin aut MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Park, Sun-Young verfasserin aut Lee, Seul Ah verfasserin aut Park, Min-Gyeong verfasserin aut Yu, Sun-Kyoung verfasserin aut Lee, Myoung-Hwa verfasserin aut Park, Mi-Ra verfasserin aut Kim, Su-Gwan verfasserin aut Oh, Ji-Su verfasserin aut Lee, Sook-Young verfasserin aut Kim, Chun Sung verfasserin aut Kim, Heung-Joong verfasserin aut Chun, Hong Sung verfasserin aut Kim, Jin-Soo verfasserin aut Moon, Sung-Min verfasserin aut Kim, Do Kyung verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 387(2013), 1-2 vom: 29. Okt., Seite 71-79 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 https://dx.doi.org/10.1007/s11010-013-1872-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 387 2013 1-2 29 10 71-79 |
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10.1007/s11010-013-1872-7 doi (DE-627)SPR015643190 (SPR)s11010-013-1872-7-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Kim, Jae-Sung verfasserin aut MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Park, Sun-Young verfasserin aut Lee, Seul Ah verfasserin aut Park, Min-Gyeong verfasserin aut Yu, Sun-Kyoung verfasserin aut Lee, Myoung-Hwa verfasserin aut Park, Mi-Ra verfasserin aut Kim, Su-Gwan verfasserin aut Oh, Ji-Su verfasserin aut Lee, Sook-Young verfasserin aut Kim, Chun Sung verfasserin aut Kim, Heung-Joong verfasserin aut Chun, Hong Sung verfasserin aut Kim, Jin-Soo verfasserin aut Moon, Sung-Min verfasserin aut Kim, Do Kyung verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 387(2013), 1-2 vom: 29. Okt., Seite 71-79 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 https://dx.doi.org/10.1007/s11010-013-1872-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 387 2013 1-2 29 10 71-79 |
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Enthalten in Molecular and cellular biochemistry 387(2013), 1-2 vom: 29. Okt., Seite 71-79 volume:387 year:2013 number:1-2 day:29 month:10 pages:71-79 |
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MicroRNA (miRNA) AXIN-2 Oral carcinoma Oncogenic activity Apoptosis |
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Kim, Jae-Sung @@aut@@ Park, Sun-Young @@aut@@ Lee, Seul Ah @@aut@@ Park, Min-Gyeong @@aut@@ Yu, Sun-Kyoung @@aut@@ Lee, Myoung-Hwa @@aut@@ Park, Mi-Ra @@aut@@ Kim, Su-Gwan @@aut@@ Oh, Ji-Su @@aut@@ Lee, Sook-Young @@aut@@ Kim, Chun Sung @@aut@@ Kim, Heung-Joong @@aut@@ Chun, Hong Sung @@aut@@ Kim, Jin-Soo @@aut@@ Moon, Sung-Min @@aut@@ Kim, Do Kyung @@aut@@ |
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2013-10-29T00:00:00Z |
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| author |
Kim, Jae-Sung |
| spellingShingle |
Kim, Jae-Sung ddc 540 bkl 44.00 misc MicroRNA (miRNA) misc AXIN-2 misc Oral carcinoma misc Oncogenic activity misc Apoptosis MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
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540 ASE 44.00 bkl MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell MicroRNA (miRNA) (dpeaa)DE-He213 AXIN-2 (dpeaa)DE-He213 Oral carcinoma (dpeaa)DE-He213 Oncogenic activity (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 |
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ddc 540 bkl 44.00 misc MicroRNA (miRNA) misc AXIN-2 misc Oral carcinoma misc Oncogenic activity misc Apoptosis |
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ddc 540 bkl 44.00 misc MicroRNA (miRNA) misc AXIN-2 misc Oral carcinoma misc Oncogenic activity misc Apoptosis |
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ddc 540 bkl 44.00 misc MicroRNA (miRNA) misc AXIN-2 misc Oral carcinoma misc Oncogenic activity misc Apoptosis |
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MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
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(DE-627)SPR015643190 (SPR)s11010-013-1872-7-e |
| title_full |
MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
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Kim, Jae-Sung |
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Molecular and cellular biochemistry |
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Kim, Jae-Sung Park, Sun-Young Lee, Seul Ah Park, Min-Gyeong Yu, Sun-Kyoung Lee, Myoung-Hwa Park, Mi-Ra Kim, Su-Gwan Oh, Ji-Su Lee, Sook-Young Kim, Chun Sung Kim, Heung-Joong Chun, Hong Sung Kim, Jin-Soo Moon, Sung-Min Kim, Do Kyung |
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Kim, Jae-Sung |
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10.1007/s11010-013-1872-7 |
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540 |
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verfasserin |
| title_sort |
microrna-205 suppresses the oral carcinoma oncogenic activity via down-regulation of axin-2 in kb human oral cancer cell |
| title_auth |
MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
| abstract |
Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. |
| abstractGer |
Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. |
| abstract_unstemmed |
Abstract MicroRNA (miRNA) is a small noncoding RNA molecule, 19–25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33 % in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50 % by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3′UTR (64–92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy. |
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| title_short |
MicroRNA-205 suppresses the oral carcinoma oncogenic activity via down-regulation of Axin-2 in KB human oral cancer cell |
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https://dx.doi.org/10.1007/s11010-013-1872-7 |
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Park, Sun-Young Lee, Seul Ah Park, Min-Gyeong Yu, Sun-Kyoung Lee, Myoung-Hwa Park, Mi-Ra Kim, Su-Gwan Oh, Ji-Su Lee, Sook-Young Kim, Chun Sung Kim, Heung-Joong Chun, Hong Sung Kim, Jin-Soo Moon, Sung-Min Kim, Do Kyung |
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Park, Sun-Young Lee, Seul Ah Park, Min-Gyeong Yu, Sun-Kyoung Lee, Myoung-Hwa Park, Mi-Ra Kim, Su-Gwan Oh, Ji-Su Lee, Sook-Young Kim, Chun Sung Kim, Heung-Joong Chun, Hong Sung Kim, Jin-Soo Moon, Sung-Min Kim, Do Kyung |
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10.1007/s11010-013-1872-7 |
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2024-07-03T17:37:10.604Z |
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