P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1
The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systema...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Laudato, Sara - 1988- [verfasserIn] Patil, Nitin - 1976- [verfasserIn] Abba, Mohammed L. - 1974- [verfasserIn] Leupold, Jörg - 1969- [verfasserIn] Gaiser, Timo - 1975- [verfasserIn] Marx, Alexander - 1956- [verfasserIn] Allgayer, Heike - 1969- [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Anmerkung: |
Gesehen am 27.06.2018 |
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| Umfang: |
12 |
| Übergeordnetes Werk: |
Enthalten in: International journal of cancer - Bognor Regis : Wiley-Liss, 1966, 141(2017), 9, Seite 1879-1890 |
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| Übergeordnetes Werk: |
volume:141 ; year:2017 ; number:9 ; pages:1879-1890 ; extent:12 |
| Links: |
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| DOI / URN: |
10.1002/ijc.30854 |
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| Katalog-ID: |
1576919676 |
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| 245 | 1 | 0 | |a P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 |c Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer |
| 264 | 1 | |c 2017 | |
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| 520 | |a The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. | ||
| 650 | 4 | |a cancer | |
| 650 | 4 | |a integrins | |
| 650 | 4 | |a metastasis | |
| 650 | 4 | |a microRNAs | |
| 650 | 4 | |a miR-30e | |
| 650 | 4 | |a P53 | |
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10.1002/ijc.30854 doi (DE-627)1576919676 (DE-576)506919676 (DE-599)BSZ506919676 (OCoLC)1341013012 DE-627 ger DE-627 rda eng Laudato, Sara 1988- verfasserin (DE-588)1129464660 (DE-627)884022471 (DE-576)486407985 aut P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer 2017 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 27.06.2018 The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. cancer integrins metastasis microRNAs miR-30e P53 Patil, Nitin 1976- verfasserin (DE-588)1031802177 (DE-627)747795371 (DE-576)379534622 aut Abba, Mohammed L. 1974- verfasserin (DE-588)1024986101 (DE-627)720854369 (DE-576)369801407 aut Leupold, Jörg 1969- verfasserin (DE-588)130056030 (DE-627)488795796 (DE-576)29797310X aut Gaiser, Timo 1975- verfasserin (DE-588)1030402280 (DE-627)735221685 (DE-576)378226533 aut Marx, Alexander 1956- verfasserin (DE-588)122478258 (DE-627)705923673 (DE-576)214254488 aut Allgayer, Heike 1969- verfasserin (DE-588)1024987884 (DE-627)720854466 (DE-576)369805003 aut Enthalten in International journal of cancer Bognor Regis : Wiley-Liss, 1966 141(2017), 9, Seite 1879-1890 Online-Ressource (DE-627)269532781 (DE-600)1474822-8 (DE-576)079876129 1097-0215 nnns volume:141 year:2017 number:9 pages:1879-1890 extent:12 http://dx.doi.org/10.1002/ijc.30854 Verlag Resolving-System Volltext http://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.30854 Verlag 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_65 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_4367 GBV_ILN_4393 GBV_ILN_4700 AR 141 2017 9 1879-1890 12 2013 01 DE-16-250 3013915838 00 --%%-- --%%-- --%%-- --%%-- l01 27-06-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_8 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1524969370 Patil, Nitin 2013 01 DE-16-250 04 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1439807345 Abba, Mohammed L. 2013 01 DE-16-250 05 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1451500963 Leupold, Jörg 2013 01 DE-16-250 06 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1448227135 Gaiser, Timo 2013 01 DE-16-250 07 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)144770293X Marx, Alexander 2013 01 DE-16-250 08 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_7 2013 01 DE-16-250 09 p (DE-627)1439807183 Allgayer, Heike 2013 01 DE-16-250 09 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_8 |
| spelling |
10.1002/ijc.30854 doi (DE-627)1576919676 (DE-576)506919676 (DE-599)BSZ506919676 (OCoLC)1341013012 DE-627 ger DE-627 rda eng Laudato, Sara 1988- verfasserin (DE-588)1129464660 (DE-627)884022471 (DE-576)486407985 aut P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer 2017 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 27.06.2018 The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. cancer integrins metastasis microRNAs miR-30e P53 Patil, Nitin 1976- verfasserin (DE-588)1031802177 (DE-627)747795371 (DE-576)379534622 aut Abba, Mohammed L. 1974- verfasserin (DE-588)1024986101 (DE-627)720854369 (DE-576)369801407 aut Leupold, Jörg 1969- verfasserin (DE-588)130056030 (DE-627)488795796 (DE-576)29797310X aut Gaiser, Timo 1975- verfasserin (DE-588)1030402280 (DE-627)735221685 (DE-576)378226533 aut Marx, Alexander 1956- verfasserin (DE-588)122478258 (DE-627)705923673 (DE-576)214254488 aut Allgayer, Heike 1969- verfasserin (DE-588)1024987884 (DE-627)720854466 (DE-576)369805003 aut Enthalten in International journal of cancer Bognor Regis : Wiley-Liss, 1966 141(2017), 9, Seite 1879-1890 Online-Ressource (DE-627)269532781 (DE-600)1474822-8 (DE-576)079876129 1097-0215 nnns volume:141 year:2017 number:9 pages:1879-1890 extent:12 http://dx.doi.org/10.1002/ijc.30854 Verlag Resolving-System Volltext http://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.30854 Verlag 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_65 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_4367 GBV_ILN_4393 GBV_ILN_4700 AR 141 2017 9 1879-1890 12 2013 01 DE-16-250 3013915838 00 --%%-- --%%-- --%%-- --%%-- l01 27-06-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_8 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1524969370 Patil, Nitin 2013 01 DE-16-250 04 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1439807345 Abba, Mohammed L. 2013 01 DE-16-250 05 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1451500963 Leupold, Jörg 2013 01 DE-16-250 06 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1448227135 Gaiser, Timo 2013 01 DE-16-250 07 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)144770293X Marx, Alexander 2013 01 DE-16-250 08 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_7 2013 01 DE-16-250 09 p (DE-627)1439807183 Allgayer, Heike 2013 01 DE-16-250 09 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_8 |
| allfields_unstemmed |
10.1002/ijc.30854 doi (DE-627)1576919676 (DE-576)506919676 (DE-599)BSZ506919676 (OCoLC)1341013012 DE-627 ger DE-627 rda eng Laudato, Sara 1988- verfasserin (DE-588)1129464660 (DE-627)884022471 (DE-576)486407985 aut P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer 2017 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 27.06.2018 The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. cancer integrins metastasis microRNAs miR-30e P53 Patil, Nitin 1976- verfasserin (DE-588)1031802177 (DE-627)747795371 (DE-576)379534622 aut Abba, Mohammed L. 1974- verfasserin (DE-588)1024986101 (DE-627)720854369 (DE-576)369801407 aut Leupold, Jörg 1969- verfasserin (DE-588)130056030 (DE-627)488795796 (DE-576)29797310X aut Gaiser, Timo 1975- verfasserin (DE-588)1030402280 (DE-627)735221685 (DE-576)378226533 aut Marx, Alexander 1956- verfasserin (DE-588)122478258 (DE-627)705923673 (DE-576)214254488 aut Allgayer, Heike 1969- verfasserin (DE-588)1024987884 (DE-627)720854466 (DE-576)369805003 aut Enthalten in International journal of cancer Bognor Regis : Wiley-Liss, 1966 141(2017), 9, Seite 1879-1890 Online-Ressource (DE-627)269532781 (DE-600)1474822-8 (DE-576)079876129 1097-0215 nnns volume:141 year:2017 number:9 pages:1879-1890 extent:12 http://dx.doi.org/10.1002/ijc.30854 Verlag Resolving-System Volltext http://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.30854 Verlag 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_65 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_4367 GBV_ILN_4393 GBV_ILN_4700 AR 141 2017 9 1879-1890 12 2013 01 DE-16-250 3013915838 00 --%%-- --%%-- --%%-- --%%-- l01 27-06-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_8 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1524969370 Patil, Nitin 2013 01 DE-16-250 04 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1439807345 Abba, Mohammed L. 2013 01 DE-16-250 05 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1451500963 Leupold, Jörg 2013 01 DE-16-250 06 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1448227135 Gaiser, Timo 2013 01 DE-16-250 07 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)144770293X Marx, Alexander 2013 01 DE-16-250 08 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_7 2013 01 DE-16-250 09 p (DE-627)1439807183 Allgayer, Heike 2013 01 DE-16-250 09 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_8 |
| allfieldsGer |
10.1002/ijc.30854 doi (DE-627)1576919676 (DE-576)506919676 (DE-599)BSZ506919676 (OCoLC)1341013012 DE-627 ger DE-627 rda eng Laudato, Sara 1988- verfasserin (DE-588)1129464660 (DE-627)884022471 (DE-576)486407985 aut P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer 2017 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 27.06.2018 The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. cancer integrins metastasis microRNAs miR-30e P53 Patil, Nitin 1976- verfasserin (DE-588)1031802177 (DE-627)747795371 (DE-576)379534622 aut Abba, Mohammed L. 1974- verfasserin (DE-588)1024986101 (DE-627)720854369 (DE-576)369801407 aut Leupold, Jörg 1969- verfasserin (DE-588)130056030 (DE-627)488795796 (DE-576)29797310X aut Gaiser, Timo 1975- verfasserin (DE-588)1030402280 (DE-627)735221685 (DE-576)378226533 aut Marx, Alexander 1956- verfasserin (DE-588)122478258 (DE-627)705923673 (DE-576)214254488 aut Allgayer, Heike 1969- verfasserin (DE-588)1024987884 (DE-627)720854466 (DE-576)369805003 aut Enthalten in International journal of cancer Bognor Regis : Wiley-Liss, 1966 141(2017), 9, Seite 1879-1890 Online-Ressource (DE-627)269532781 (DE-600)1474822-8 (DE-576)079876129 1097-0215 nnns volume:141 year:2017 number:9 pages:1879-1890 extent:12 http://dx.doi.org/10.1002/ijc.30854 Verlag Resolving-System Volltext http://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.30854 Verlag 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_65 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_4367 GBV_ILN_4393 GBV_ILN_4700 AR 141 2017 9 1879-1890 12 2013 01 DE-16-250 3013915838 00 --%%-- --%%-- --%%-- --%%-- l01 27-06-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_8 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1524969370 Patil, Nitin 2013 01 DE-16-250 04 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1439807345 Abba, Mohammed L. 2013 01 DE-16-250 05 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1451500963 Leupold, Jörg 2013 01 DE-16-250 06 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1448227135 Gaiser, Timo 2013 01 DE-16-250 07 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)144770293X Marx, Alexander 2013 01 DE-16-250 08 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_7 2013 01 DE-16-250 09 p (DE-627)1439807183 Allgayer, Heike 2013 01 DE-16-250 09 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_8 |
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10.1002/ijc.30854 doi (DE-627)1576919676 (DE-576)506919676 (DE-599)BSZ506919676 (OCoLC)1341013012 DE-627 ger DE-627 rda eng Laudato, Sara 1988- verfasserin (DE-588)1129464660 (DE-627)884022471 (DE-576)486407985 aut P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer 2017 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 27.06.2018 The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. cancer integrins metastasis microRNAs miR-30e P53 Patil, Nitin 1976- verfasserin (DE-588)1031802177 (DE-627)747795371 (DE-576)379534622 aut Abba, Mohammed L. 1974- verfasserin (DE-588)1024986101 (DE-627)720854369 (DE-576)369801407 aut Leupold, Jörg 1969- verfasserin (DE-588)130056030 (DE-627)488795796 (DE-576)29797310X aut Gaiser, Timo 1975- verfasserin (DE-588)1030402280 (DE-627)735221685 (DE-576)378226533 aut Marx, Alexander 1956- verfasserin (DE-588)122478258 (DE-627)705923673 (DE-576)214254488 aut Allgayer, Heike 1969- verfasserin (DE-588)1024987884 (DE-627)720854466 (DE-576)369805003 aut Enthalten in International journal of cancer Bognor Regis : Wiley-Liss, 1966 141(2017), 9, Seite 1879-1890 Online-Ressource (DE-627)269532781 (DE-600)1474822-8 (DE-576)079876129 1097-0215 nnns volume:141 year:2017 number:9 pages:1879-1890 extent:12 http://dx.doi.org/10.1002/ijc.30854 Verlag Resolving-System Volltext http://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.30854 Verlag 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_65 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_4367 GBV_ILN_4393 GBV_ILN_4700 AR 141 2017 9 1879-1890 12 2013 01 DE-16-250 3013915838 00 --%%-- --%%-- --%%-- --%%-- l01 27-06-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_8 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1524969370 Patil, Nitin 2013 01 DE-16-250 04 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1439807345 Abba, Mohammed L. 2013 01 DE-16-250 05 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1451500963 Leupold, Jörg 2013 01 DE-16-250 06 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1448227135 Gaiser, Timo 2013 01 DE-16-250 07 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)144770293X Marx, Alexander 2013 01 DE-16-250 08 k (DE-627)141646882X Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_7 2013 01 DE-16-250 09 p (DE-627)1439807183 Allgayer, Heike 2013 01 DE-16-250 09 k (DE-627)1416469214 Zentrum für Biomedizin und Medizintechnik Mannheim (CBTM) 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_8 |
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Laudato, Sara @@aut@@ Patil, Nitin @@aut@@ Abba, Mohammed L. @@aut@@ Leupold, Jörg @@aut@@ Gaiser, Timo @@aut@@ Marx, Alexander @@aut@@ Allgayer, Heike @@aut@@ |
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P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 |
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P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 Sara Laudato, Nitin Patil, Mohammed L. Abba, Joerg H. Leupold, Axel Benner, Timo Gaiser, Alexander Marx and Heike Allgayer |
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p53-induced mir-30e-5p inhibits colorectal cancer invasion and metastasis by targeting itga6 and itgb1 |
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P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1 |
| abstract |
The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. Gesehen am 27.06.2018 |
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The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. Gesehen am 27.06.2018 |
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The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis. Gesehen am 27.06.2018 |
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