Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development
MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17...
Ausführliche Beschreibung
Autor*in: |
Shigoka, Masatoshi [verfasserIn] Tsuchida, Akihiko [verfasserIn] Matsudo, Takaaki [verfasserIn] Nagakawa, Yuichi [verfasserIn] Saito, Hitoshi [verfasserIn] Suzuki, Yoshiaki [verfasserIn] Aoki, Tatsuya [verfasserIn] Murakami, Yoshiki [verfasserIn] Toyoda, Hidenori [verfasserIn] Kumada, Takashi [verfasserIn] Bartenschlager, Ralf - 1958- [verfasserIn] Kato, Nobuyuki [verfasserIn] Ikeda, Masanori [verfasserIn] Takashina, Tomoki [verfasserIn] Tanaka, Masami [verfasserIn] Suzuki, Rieko [verfasserIn] Oikawa, Kosuke [verfasserIn] Takanashi, Masakatsu [verfasserIn] Kuroda, Masahiko [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
29 April 2010 |
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Schlagwörter: |
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Anmerkung: |
Gesehen am 17.07.2023 |
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Umfang: |
7 |
Übergeordnetes Werk: |
Enthalten in: Pathology international - Oxford [u.a.] : Wiley-Blackwell, 1951, 60(2010), 5, Seite 351-357 |
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Übergeordnetes Werk: |
volume:60 ; year:2010 ; number:5 ; pages:351-357 ; extent:7 |
Links: |
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DOI / URN: |
10.1111/j.1440-1827.2010.02526.x |
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Katalog-ID: |
1852825464 |
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245 | 1 | 0 | |a Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development |c Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda |
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520 | |a MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. | ||
650 | 4 | |a hepatocellular carcinoma | |
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650 | 4 | |a miR-638 | |
650 | 4 | |a miR-92a | |
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700 | 1 | |a Tsuchida, Akihiko |e verfasserin |4 aut | |
700 | 1 | |a Matsudo, Takaaki |e verfasserin |4 aut | |
700 | 1 | |a Nagakawa, Yuichi |e verfasserin |4 aut | |
700 | 1 | |a Saito, Hitoshi |e verfasserin |4 aut | |
700 | 1 | |a Suzuki, Yoshiaki |e verfasserin |4 aut | |
700 | 1 | |a Aoki, Tatsuya |e verfasserin |4 aut | |
700 | 1 | |a Murakami, Yoshiki |e verfasserin |4 aut | |
700 | 1 | |a Toyoda, Hidenori |e verfasserin |4 aut | |
700 | 1 | |a Kumada, Takashi |e verfasserin |4 aut | |
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700 | 1 | |a Kato, Nobuyuki |e verfasserin |4 aut | |
700 | 1 | |a Ikeda, Masanori |e verfasserin |4 aut | |
700 | 1 | |a Takashina, Tomoki |e verfasserin |4 aut | |
700 | 1 | |a Tanaka, Masami |e verfasserin |4 aut | |
700 | 1 | |a Suzuki, Rieko |e verfasserin |4 aut | |
700 | 1 | |a Oikawa, Kosuke |e verfasserin |4 aut | |
700 | 1 | |a Takanashi, Masakatsu |e verfasserin |4 aut | |
700 | 1 | |a Kuroda, Masahiko |e verfasserin |4 aut | |
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10.1111/j.1440-1827.2010.02526.x doi (DE-627)1852825464 (DE-599)KXP1852825464 (OCoLC)1425876858 DE-627 ger DE-627 rda eng Shigoka, Masatoshi verfasserin (DE-588)1296387097 (DE-627)1852825235 aut Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda 29 April 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 17.07.2023 MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. hepatocellular carcinoma microRNA miR-638 miR-92a plasma Tsuchida, Akihiko verfasserin aut Matsudo, Takaaki verfasserin aut Nagakawa, Yuichi verfasserin aut Saito, Hitoshi verfasserin aut Suzuki, Yoshiaki verfasserin aut Aoki, Tatsuya verfasserin aut Murakami, Yoshiki verfasserin aut Toyoda, Hidenori verfasserin aut Kumada, Takashi verfasserin aut Bartenschlager, Ralf 1958- verfasserin (DE-588)1058097989 (DE-627)796390509 (DE-576)168706067 aut Kato, Nobuyuki verfasserin aut Ikeda, Masanori verfasserin aut Takashina, Tomoki verfasserin aut Tanaka, Masami verfasserin aut Suzuki, Rieko verfasserin aut Oikawa, Kosuke verfasserin aut Takanashi, Masakatsu verfasserin aut Kuroda, Masahiko verfasserin aut Enthalten in Pathology international Oxford [u.a.] : Wiley-Blackwell, 1951 60(2010), 5, Seite 351-357 Online-Ressource (DE-627)320471322 (DE-600)2008574-6 (DE-576)091169623 1440-1827 nnns volume:60 year:2010 number:5 pages:351-357 extent:7 https://doi.org/10.1111/j.1440-1827.2010.02526.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2010 5 351-357 7 2013 01 DE-16-250 4354335484 00 --%%-- --%%-- --%%-- --%%-- l01 17-07-23 2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
spelling |
10.1111/j.1440-1827.2010.02526.x doi (DE-627)1852825464 (DE-599)KXP1852825464 (OCoLC)1425876858 DE-627 ger DE-627 rda eng Shigoka, Masatoshi verfasserin (DE-588)1296387097 (DE-627)1852825235 aut Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda 29 April 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 17.07.2023 MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. hepatocellular carcinoma microRNA miR-638 miR-92a plasma Tsuchida, Akihiko verfasserin aut Matsudo, Takaaki verfasserin aut Nagakawa, Yuichi verfasserin aut Saito, Hitoshi verfasserin aut Suzuki, Yoshiaki verfasserin aut Aoki, Tatsuya verfasserin aut Murakami, Yoshiki verfasserin aut Toyoda, Hidenori verfasserin aut Kumada, Takashi verfasserin aut Bartenschlager, Ralf 1958- verfasserin (DE-588)1058097989 (DE-627)796390509 (DE-576)168706067 aut Kato, Nobuyuki verfasserin aut Ikeda, Masanori verfasserin aut Takashina, Tomoki verfasserin aut Tanaka, Masami verfasserin aut Suzuki, Rieko verfasserin aut Oikawa, Kosuke verfasserin aut Takanashi, Masakatsu verfasserin aut Kuroda, Masahiko verfasserin aut Enthalten in Pathology international Oxford [u.a.] : Wiley-Blackwell, 1951 60(2010), 5, Seite 351-357 Online-Ressource (DE-627)320471322 (DE-600)2008574-6 (DE-576)091169623 1440-1827 nnns volume:60 year:2010 number:5 pages:351-357 extent:7 https://doi.org/10.1111/j.1440-1827.2010.02526.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2010 5 351-357 7 2013 01 DE-16-250 4354335484 00 --%%-- --%%-- --%%-- --%%-- l01 17-07-23 2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
allfields_unstemmed |
10.1111/j.1440-1827.2010.02526.x doi (DE-627)1852825464 (DE-599)KXP1852825464 (OCoLC)1425876858 DE-627 ger DE-627 rda eng Shigoka, Masatoshi verfasserin (DE-588)1296387097 (DE-627)1852825235 aut Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda 29 April 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 17.07.2023 MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. hepatocellular carcinoma microRNA miR-638 miR-92a plasma Tsuchida, Akihiko verfasserin aut Matsudo, Takaaki verfasserin aut Nagakawa, Yuichi verfasserin aut Saito, Hitoshi verfasserin aut Suzuki, Yoshiaki verfasserin aut Aoki, Tatsuya verfasserin aut Murakami, Yoshiki verfasserin aut Toyoda, Hidenori verfasserin aut Kumada, Takashi verfasserin aut Bartenschlager, Ralf 1958- verfasserin (DE-588)1058097989 (DE-627)796390509 (DE-576)168706067 aut Kato, Nobuyuki verfasserin aut Ikeda, Masanori verfasserin aut Takashina, Tomoki verfasserin aut Tanaka, Masami verfasserin aut Suzuki, Rieko verfasserin aut Oikawa, Kosuke verfasserin aut Takanashi, Masakatsu verfasserin aut Kuroda, Masahiko verfasserin aut Enthalten in Pathology international Oxford [u.a.] : Wiley-Blackwell, 1951 60(2010), 5, Seite 351-357 Online-Ressource (DE-627)320471322 (DE-600)2008574-6 (DE-576)091169623 1440-1827 nnns volume:60 year:2010 number:5 pages:351-357 extent:7 https://doi.org/10.1111/j.1440-1827.2010.02526.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2010 5 351-357 7 2013 01 DE-16-250 4354335484 00 --%%-- --%%-- --%%-- --%%-- l01 17-07-23 2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
allfieldsGer |
10.1111/j.1440-1827.2010.02526.x doi (DE-627)1852825464 (DE-599)KXP1852825464 (OCoLC)1425876858 DE-627 ger DE-627 rda eng Shigoka, Masatoshi verfasserin (DE-588)1296387097 (DE-627)1852825235 aut Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda 29 April 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 17.07.2023 MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. hepatocellular carcinoma microRNA miR-638 miR-92a plasma Tsuchida, Akihiko verfasserin aut Matsudo, Takaaki verfasserin aut Nagakawa, Yuichi verfasserin aut Saito, Hitoshi verfasserin aut Suzuki, Yoshiaki verfasserin aut Aoki, Tatsuya verfasserin aut Murakami, Yoshiki verfasserin aut Toyoda, Hidenori verfasserin aut Kumada, Takashi verfasserin aut Bartenschlager, Ralf 1958- verfasserin (DE-588)1058097989 (DE-627)796390509 (DE-576)168706067 aut Kato, Nobuyuki verfasserin aut Ikeda, Masanori verfasserin aut Takashina, Tomoki verfasserin aut Tanaka, Masami verfasserin aut Suzuki, Rieko verfasserin aut Oikawa, Kosuke verfasserin aut Takanashi, Masakatsu verfasserin aut Kuroda, Masahiko verfasserin aut Enthalten in Pathology international Oxford [u.a.] : Wiley-Blackwell, 1951 60(2010), 5, Seite 351-357 Online-Ressource (DE-627)320471322 (DE-600)2008574-6 (DE-576)091169623 1440-1827 nnns volume:60 year:2010 number:5 pages:351-357 extent:7 https://doi.org/10.1111/j.1440-1827.2010.02526.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2010 5 351-357 7 2013 01 DE-16-250 4354335484 00 --%%-- --%%-- --%%-- --%%-- l01 17-07-23 2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
allfieldsSound |
10.1111/j.1440-1827.2010.02526.x doi (DE-627)1852825464 (DE-599)KXP1852825464 (OCoLC)1425876858 DE-627 ger DE-627 rda eng Shigoka, Masatoshi verfasserin (DE-588)1296387097 (DE-627)1852825235 aut Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda 29 April 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 17.07.2023 MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. hepatocellular carcinoma microRNA miR-638 miR-92a plasma Tsuchida, Akihiko verfasserin aut Matsudo, Takaaki verfasserin aut Nagakawa, Yuichi verfasserin aut Saito, Hitoshi verfasserin aut Suzuki, Yoshiaki verfasserin aut Aoki, Tatsuya verfasserin aut Murakami, Yoshiki verfasserin aut Toyoda, Hidenori verfasserin aut Kumada, Takashi verfasserin aut Bartenschlager, Ralf 1958- verfasserin (DE-588)1058097989 (DE-627)796390509 (DE-576)168706067 aut Kato, Nobuyuki verfasserin aut Ikeda, Masanori verfasserin aut Takashina, Tomoki verfasserin aut Tanaka, Masami verfasserin aut Suzuki, Rieko verfasserin aut Oikawa, Kosuke verfasserin aut Takanashi, Masakatsu verfasserin aut Kuroda, Masahiko verfasserin aut Enthalten in Pathology international Oxford [u.a.] : Wiley-Blackwell, 1951 60(2010), 5, Seite 351-357 Online-Ressource (DE-627)320471322 (DE-600)2008574-6 (DE-576)091169623 1440-1827 nnns volume:60 year:2010 number:5 pages:351-357 extent:7 https://doi.org/10.1111/j.1440-1827.2010.02526.x Verlag Resolving-System lizenzpflichtig Volltext https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x Verlag lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2010 5 351-357 7 2013 01 DE-16-250 4354335484 00 --%%-- --%%-- --%%-- --%%-- l01 17-07-23 2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
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Shigoka, Masatoshi @@aut@@ Tsuchida, Akihiko @@aut@@ Matsudo, Takaaki @@aut@@ Nagakawa, Yuichi @@aut@@ Saito, Hitoshi @@aut@@ Suzuki, Yoshiaki @@aut@@ Aoki, Tatsuya @@aut@@ Murakami, Yoshiki @@aut@@ Toyoda, Hidenori @@aut@@ Kumada, Takashi @@aut@@ Bartenschlager, Ralf @@aut@@ Kato, Nobuyuki @@aut@@ Ikeda, Masanori @@aut@@ Takashina, Tomoki @@aut@@ Tanaka, Masami @@aut@@ Suzuki, Rieko @@aut@@ Oikawa, Kosuke @@aut@@ Takanashi, Masakatsu @@aut@@ Kuroda, Masahiko @@aut@@ |
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2013 01 DE-16-250 00 s hd2010 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_19 2013 01 DE-16-250 03 s s_7 2013 01 DE-16-250 04 p (DE-627)1484102681 Bartenschlager, Ralf 2013 01 DE-16-250 04 k (DE-627)1416741526 Department für Infektiologie 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda hepatocellular carcinoma microRNA miR-638 miR-92a plasma |
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Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development Masatoshi Shigoka, Akihiko Tsuchida, Takaaki Matsudo, Yuichi Nagakawa, Hitoshi Saito, Yoshiaki Suzuki, Tatsuya Aoki, Yoshiki Murakami, Hidenori Toyoda, Takashi Kumada, Ralf Bartenschlager, Nobuyuki Kato, Masanori Ikeda, Tomoki Takashina, Masami Tanaka, Rieko Suzuki, Kosuke Oikawa, Masakatsu Takanashi and Masahiko Kuroda |
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Shigoka, Masatoshi Tsuchida, Akihiko Matsudo, Takaaki Nagakawa, Yuichi Saito, Hitoshi Suzuki, Yoshiaki Aoki, Tatsuya Murakami, Yoshiki Toyoda, Hidenori Kumada, Takashi Bartenschlager, Ralf Kato, Nobuyuki Ikeda, Masanori Takashina, Tomoki Tanaka, Masami Suzuki, Rieko Oikawa, Kosuke Takanashi, Masakatsu Kuroda, Masahiko |
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deregulation of mir-92a expression is implicated in hepatocellular carcinoma development |
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Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development |
abstract |
MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. Gesehen am 17.07.2023 |
abstractGer |
MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. Gesehen am 17.07.2023 |
abstract_unstemmed |
MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC. Gesehen am 17.07.2023 |
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container_issue |
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title_short |
Deregulation of miR-92a expression is implicated in hepatocellular carcinoma development |
url |
https://doi.org/10.1111/j.1440-1827.2010.02526.x https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1827.2010.02526.x |
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Tsuchida, Akihiko Matsudo, Takaaki Nagakawa, Yuichi Saito, Hitoshi Suzuki, Yoshiaki Aoki, Tatsuya Murakami, Yoshiki Toyoda, Hidenori Kumada, Takashi Bartenschlager, Ralf 1958- Kato, Nobuyuki Ikeda, Masanori Takashina, Tomoki Tanaka, Masami Suzuki, Rieko Oikawa, Kosuke Takanashi, Masakatsu Kuroda, Masahiko |
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up_date |
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