MicroRNAs regulate critical genes associated with multiple myeloma pathogenesis
Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in t...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 105; no. 35; pp. 12885 - 12890 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
02.09.2008
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b~25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17~92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17~92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b~25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. |
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| AbstractList | Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b~25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17~92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17~92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b~25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b approximately 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17 approximately 92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17 approximately 92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b approximately 25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis.Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b approximately 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17 approximately 92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17 approximately 92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b approximately 25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b∼25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17∼92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17∼92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b∼25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b approximately 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17 approximately 92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17 approximately 92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b approximately 25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106b~25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17~92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17~92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b~25 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. [PUBLICATION ABSTRACT] Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines (n = 49) and CD138+ bone marrow PCs from subjects with MM (n = 16), monoclonal gammopathy of undetermined significance (MGUS) (n = 6), and normal donors (n = 6). We identified overexpression of miR-21, miR-106ba1/425 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17a1/492 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b, that are part of the miR-17a1/492 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106ba1/425 cluster, miR-181a and b, and miR-32. Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines ( n = 49) and CD138+ bone marrow PCs from subjects with MM ( n = 16), monoclonal gammopathy of undetermined significance (MGUS) ( n = 6), and normal donors ( n = 6). We identified overexpression of miR-21 , miR-106b ∼ 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17 ∼ 92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b , that are part of the miR-17 ∼ 92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b ∼ 25 cluster, miR-181a and b , and miR-32 . Xenograft studies using human MM cell lines treated with miR-19a and b , and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small noncoding RNAs targeting multiple mRNAs, has revealed a new level of gene expression regulation. To determine whether miRNAs play a role in the malignant transformation of plasma cells (PCs), we have used both miRNA microarrays and quantitative real time PCR to profile miRNA expression in MM-derived cell lines ( n = 49) and CD138+ bone marrow PCs from subjects with MM ( n = 16), monoclonal gammopathy of undetermined significance (MGUS) ( n = 6), and normal donors ( n = 6). We identified overexpression of miR-21 , miR-106b ∼ 25 cluster, miR-181a and b in MM and MGUS samples with respect to healthy PCs. Selective up-regulation of miR-32 and miR-17 ∼ 92 cluster was identified in MM subjects and cell lines but not in MGUS subjects or healthy PCs. Furthermore, two miRNAs, miR-19a and 19b , that are part of the miR-17 ∼ 92 cluster, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a critical role as inhibitor of IL-6 growth signaling. We also identified p300-CBP-associated factor, a gene involved in p53 regulation, as a bona fide target of the miR106b ∼ 25 cluster, miR-181a and b , and miR-32 . Xenograft studies using human MM cell lines treated with miR-19a and b , and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice. In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis. PCAF SOCS-1 tumor suppressor gene MGUS plasma cells |
| Author | Palumbo, Tiziana Pichiorri, Flavia Taccioli, Cristian Suh, Sung-Suk Palumbo, Antonio Munker, Reinhold Zanesi, Nicola Garzon, Ramiro Croce, Carlo M Boccadoro, Mario Alder, Hansjuerg Kuehl, Michael Volinia, Stefano Ladetto, Marco Hagan, John P Aqeilan, Rami I Drandi, Daniela |
| Author_xml | – sequence: 1 fullname: Pichiorri, Flavia – sequence: 2 fullname: Suh, Sung-Suk – sequence: 3 fullname: Ladetto, Marco – sequence: 4 fullname: Kuehl, Michael – sequence: 5 fullname: Palumbo, Tiziana – sequence: 6 fullname: Drandi, Daniela – sequence: 7 fullname: Taccioli, Cristian – sequence: 8 fullname: Zanesi, Nicola – sequence: 9 fullname: Alder, Hansjuerg – sequence: 10 fullname: Hagan, John P – sequence: 11 fullname: Munker, Reinhold – sequence: 12 fullname: Volinia, Stefano – sequence: 13 fullname: Boccadoro, Mario – sequence: 14 fullname: Garzon, Ramiro – sequence: 15 fullname: Palumbo, Antonio – sequence: 16 fullname: Aqeilan, Rami I – sequence: 17 fullname: Croce, Carlo M |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18728182$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1038/ncb1545 10.1182/blood.V99.5.1745 10.1038/ng1536 10.1056/NEJMoa050995 10.1182/blood-2002-06-1735 10.1016/j.cell.2008.02.019 10.1016/S1470-2045(03)01195-1 10.1182/blood.V77.3.587.587 10.1182/blood.V59.1.43.43 10.1073/pnas.0800135105 10.1056/NEJMra072367 10.1053/j.gastro.2007.05.022 10.1073/pnas.0510565103 10.1038/nprot.2008.14 10.1038/sj.cdd.4402090 10.1038/nrc2189 10.1182/blood-2007-07-098749 10.1038/nature03552 10.1158/0008-5472.CAN-05-0137 10.1532/IJH97.04107 10.1016/j.ccr.2008.02.013 10.1016/S0092-8674(03)01018-3 10.1189/jlb.70.3.348 10.1182/blood.V84.8.2412.2412 10.1126/science.1091903 10.1073/pnas.0403293101 10.1038/nrc1997 10.1016/j.hoc.2007.08.010 10.1016/j.beha.2007.08.004 10.1016/S0092-8674(04)00045-5 10.4161/cc.5.1.2281 10.1016/j.ejca.2005.12.026 10.1182/blood-2007-03-081133 10.1038/sj.onc.1210186 10.1038/nature03677 |
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| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-2 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 F.P. and S.S. contributed equally to this work. Contributed by Carlo M. Croce, June 27, 2008 Author contributions: F.P., S.-S.S., M.K., T.P., D.D., C.T., N.Z., S.V., M.B., A.P., R.I.A., and C.M.C. designed research; F.P., S.-S.S., M.L., M.K., T.P., D.D., C.T., N.Z., H.A., J.P.H., R.M., S.V., and R.I.A. performed research; F.P., S.-S.S., M.L., M.K., T.P., D.D., C.T., H.A., J.P.H., R.M., S.V., M.B., R.G., A.P., R.I.A., and C.M.C. contributed new reagents/analytic tools; F.P., S.-S.S., M.K., C.T., H.A., S.V., R.G., A.P., R.I.A., and C.M.C. analyzed data; and F.P., R.G., and R.I.A. wrote the paper. |
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| References | Schiltz RL (e_1_3_3_23_2) 2000; 1470 e_1_3_3_17_2 e_1_3_3_16_2 e_1_3_3_19_2 e_1_3_3_18_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_32_2 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_10_2 e_1_3_3_31_2 Drach J (e_1_3_3_5_2) 1995; 55 e_1_3_3_6_2 e_1_3_3_8_2 e_1_3_3_7_2 Greenhalgh CJ (e_1_3_3_27_2) 2001; 70 e_1_3_3_28_2 e_1_3_3_9_2 e_1_3_3_29_2 e_1_3_3_24_2 e_1_3_3_26_2 e_1_3_3_25_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_1_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_3_2 e_1_3_3_21_2 |
| References_xml | – ident: e_1_3_3_24_2 doi: 10.1038/ncb1545 – ident: e_1_3_3_32_2 doi: 10.1182/blood.V99.5.1745 – ident: e_1_3_3_22_2 doi: 10.1038/ng1536 – ident: e_1_3_3_8_2 doi: 10.1056/NEJMoa050995 – volume: 55 start-page: 3854 year: 1995 ident: e_1_3_3_5_2 article-title: Multiple myeloma: High incidence of chromosomal aneuploidy as detected by interphase fluorescence in situ hybridization publication-title: Cancer Res – ident: e_1_3_3_28_2 doi: 10.1182/blood-2002-06-1735 – ident: e_1_3_3_19_2 doi: 10.1016/j.cell.2008.02.019 – ident: e_1_3_3_15_2 doi: 10.1016/S1470-2045(03)01195-1 – ident: e_1_3_3_29_2 doi: 10.1182/blood.V77.3.587.587 – ident: e_1_3_3_6_2 doi: 10.1182/blood.V59.1.43.43 – ident: e_1_3_3_31_2 doi: 10.1073/pnas.0800135105 – ident: e_1_3_3_11_2 doi: 10.1056/NEJMra072367 – ident: e_1_3_3_34_2 doi: 10.1053/j.gastro.2007.05.022 – ident: e_1_3_3_30_2 doi: 10.1073/pnas.0510565103 – ident: e_1_3_3_17_2 doi: 10.1038/nprot.2008.14 – ident: e_1_3_3_35_2 doi: 10.1038/sj.cdd.4402090 – volume: 1470 start-page: M37 year: 2000 ident: e_1_3_3_23_2 article-title: The PCAF acetylase complex as a potential tumor suppressor publication-title: Biochim Biophys Acta – ident: e_1_3_3_3_2 doi: 10.1038/nrc2189 – ident: e_1_3_3_9_2 doi: 10.1182/blood-2007-07-098749 – ident: e_1_3_3_18_2 doi: 10.1038/nature03552 – ident: e_1_3_3_33_2 doi: 10.1158/0008-5472.CAN-05-0137 – ident: e_1_3_3_4_2 doi: 10.1532/IJH97.04107 – ident: e_1_3_3_20_2 doi: 10.1016/j.ccr.2008.02.013 – ident: e_1_3_3_21_2 doi: 10.1016/S0092-8674(03)01018-3 – volume: 70 start-page: 348 year: 2001 ident: e_1_3_3_27_2 article-title: Negative regulation of cytokine signaling publication-title: J Leukoc Biol doi: 10.1189/jlb.70.3.348 – ident: e_1_3_3_25_2 doi: 10.1182/blood.V84.8.2412.2412 – ident: e_1_3_3_16_2 doi: 10.1126/science.1091903 – ident: e_1_3_3_37_2 doi: 10.1073/pnas.0403293101 – ident: e_1_3_3_13_2 doi: 10.1038/nrc1997 – ident: e_1_3_3_2_2 doi: 10.1016/j.hoc.2007.08.010 – ident: e_1_3_3_7_2 doi: 10.1016/j.beha.2007.08.004 – ident: e_1_3_3_10_2 doi: 10.1016/S0092-8674(04)00045-5 – ident: e_1_3_3_26_2 doi: 10.4161/cc.5.1.2281 – ident: e_1_3_3_1_2 doi: 10.1016/j.ejca.2005.12.026 – ident: e_1_3_3_14_2 doi: 10.1182/blood-2007-03-081133 – ident: e_1_3_3_12_2 doi: 10.1038/sj.onc.1210186 – ident: e_1_3_3_36_2 doi: 10.1038/nature03677 |
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| Snippet | Progress in understanding the biology of multiple myeloma (MM), a plasma cell malignancy, has been slow. The discovery of microRNAs (miRNAs), a class of small... |
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| SubjectTerms | Animals antagonists Apoptosis Regulatory Proteins - metabolism Base Sequence Bcl-2-Like Protein 11 Biological Sciences Bone marrow Cell growth Cell Line, Tumor Cell lines Cells Gene expression Gene Expression Profiling gene expression regulation Gene Expression Regulation, Neoplastic genes Genes, Neoplasm Health Humans interleukin-6 Membrane Proteins - metabolism messenger RNA Mice Mice, Nude microarray technology MicroRNA MicroRNAs - genetics MicroRNAs - metabolism Molecular Sequence Data Monoclonal Gammopathy of Undetermined Significance Multiple myeloma Multiple Myeloma - genetics Multiple Myeloma - pathology myeloma non-coding RNA Oligonucleotides p300-CBP Transcription Factors - metabolism pathogenesis Pathology Plasma cells Plasma Cells - metabolism Plasma Cells - pathology proteins Proto-Oncogene Proteins - metabolism quantitative polymerase chain reaction Receptors, Interleukin-6 - metabolism Repressor Proteins - metabolism Reproducibility of Results Reverse Transcriptase Polymerase Chain Reaction Ribonucleic acid RNA Rodents Signatures STAT3 Transcription Factor - metabolism Studies Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins - metabolism Transfection Tumor cell line Tumor Suppressor Protein p53 - metabolism Tumors Up-Regulation |
| Title | MicroRNAs regulate critical genes associated with multiple myeloma pathogenesis |
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