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1 Comprehensive Cancer Center, Ohio State University, Columbus, Ohio; 2 Dipartimento di Medicina Sperimentale e Diagnostica, e Centro Interdipartimentale per la Ricerca sul Cancro, Università di Ferrara, Ferrara, Italy; 3 Molecular Targeting Unit, Department of Experimental Oncology, Istituto Nazionale Tumori, Milan, Italy; Departments of 4 Pathology, Anatomy and Cell Biology and 5 Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania; and 6 Ce.S.I. Aging Research Center, Chieti, Italy
Requests for reprints: Carlo M. Croce, Comprehensive Cancer Center, Ohio State University, Room 445C, Wiseman Hall, 400 12th Avenue, Columbus, OH 43210. Phone: 614-292-3063; Fax: 614-292-3312; E-mail: Carlo.Croce{at}osumc.edu.
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Abstract |
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Introduction |
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22-nucleotide miRNA duplex: one strand (miRNA*) of the short-lived duplex is degraded, whereas the other strand serves as mature miRNA. In animals, single-stranded miRNA binds through partial sequence homology to the 3' untranslated region (3' UTR) of target mRNAs, and causes either block of translation or, less frequently, mRNA degradation. The discovery of this class of genes has identified a new layer of gene regulation mechanisms, which play an important role in development and in various cellular processes, such as differentiation, cell growth, and cell death (2). Deviations from normal pattern of expression may play a role in diseases, such as in neurologic disorders (3). Among human diseases, it has been shown that miRNAs are aberrantly expressed or mutated in cancer, suggesting that they may play a role as a novel class of oncogenes or tumor suppressor genes. The first evidence of involvement of miRNAs in human cancer came from molecular studies characterizing the 13q14 deletion in human chronic lymphocytic leukemia (CLL), which revealed that two miRNAs, mir-15a and mir-16-1, were the only genes within the smallest common region of deletion. The same two genes were affected by a chromosomal translocation in a CLL patient. mir-16-1 and/or mir-15a were then found down-regulated in 50% to 60% of human CLL (4). Following this initial finding, miRNA expression deregulation in human cancer has been proven in other instances. For example, miR143 and miR145 are down-regulated in colon carcinomas (5). Let-7 is down-regulated in human lung carcinomas and restoration of its expression induces cell growth inhibition in lung cancer A549 cells (6). The BIC gene, which contains the miR155, is strongly up-regulated in some Burkitt's lymphoma and several other types of lymphomas (7, 8). The findings that miRNAs have a role in human cancer is further supported by the fact that >50% of miRNA genes are located at chromosomal regions, such as fragile sites, and regions of deletion or amplification that are genetically altered in human cancer (9), suggesting that the relevance of miRNAs in human cancer may be presently underestimated.
Only recently, the possibility of analyzing the entire miRNAome has become possible by the development of microarrays containing all known human miRNAs (10–15). The use of miRNA microarrays made possible to confirm miR-16 deregulation in human CLL, but also recognize miRNA expression signatures associated with well-defined clinicopathologic features of human CLL (16). Recognition of miRNAs that are differentially expressed between normal and tumor samples may help to identify those that are involved in human cancer and establish the basis to unravel their pathogenic role. Here, we present results of a genome-wide miRNA expression profiling in a large set of normal and tumor breast tissues demonstrating the existence of a breast cancer–specific miRNA signature.
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Materials and Methods |
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Immunohistochemical analysis of breast cancer samples. Hormonal receptors were evaluated with 6F11 antibody for estrogen receptor 
and PGR-1A6 for progesterone receptor (Ventana, Tucson, AZ). The proliferation index was assessed with MIB1 antibody (DAKO, Copenhagen, Denmark). ERBB2 was detected with CB11 (Ventana) and p53 protein expression was examined with DO7 (Ventana). Staining procedures were done as described (17). Only tumor cells with distinct nuclear immunostaining for estrogen receptor, progesterone receptor, Mib1, and p53 were recorded as positive. Tumor cells were considered positive for ERBB2 when they showed distinct membrane immunoreactivity. To perform a quantitative evaluation of biological markers, the Eureka Menarini computerized image analysis system was used. For each tumor section, at least 20 microscopic fields of invasive carcinoma (40x objective) were measured. The following cutoff values were used: 10% of positive nuclear area for estrogen receptor, progesterone receptor, c-erbB2, and p53; 13% of nuclei expressing Mib1 was introduced to discriminate cases with high and low proliferative activity.
MicroRNA microarray. Total RNA isolation was done with Trizol (Invitrogen, Carlsbad, CA) according to the instructions of the manufacturer. RNA labeling and hybridization on miRNA microarray chips was done as previously described (10). Briefly, 5 µg of RNA from each sample was biotin-labeled during reverse transcription using random examers. Hybridization was carried out on miRNA microarray chip (KCI version 1.0; ref. 10), which contains 368 probes, including 245 human and mouse miRNA genes, in triplicate. Hybridization signals were detected by biotin binding of a Streptavidin–Alexa 647 conjugate using a Perkin-Elmer ScanArray XL5K. Scanner images were quantified by the Quantarray software (Perkin-Elmer, Wellesley, MA).
Statistical and bioinformatic analysis of microarray data. Raw data were normalized and analyzed using the GeneSpring software version 7.2 (Silicon Genetics, Redwood City, CA). Expression data were median centered. Statistical comparisons were done by ANOVA, using the Benjamini and Hochberg correction for false-positive reductions. Prognostic miRNAs for tumor versus normal class prediction were determined by using both the Prediction Analysis of Microarrays software (PAM; ref. 18)7 and the Support Vector Machine (19) tool. Both algorithms were used for cross-validation and test-set prediction. All data were submitted using MIAMExpress to the Array Express database (accession numbers to be received upon revision).
Northern blotting. Northern blot analysis was done as previously described (4). RNA samples (10 mg each) were electrophoresed on 15% acrylamide, 7 mol/L urea Criterion precasted gels (Bio-Rad, Hercules, CA) and transferred onto Hybond-N+ membrane (Amersham Biosciences, Piscataway, NJ). Hybridization was done at 37°C in 7% SDS/0.2 mol/L Na2PO4 (pH 7.0) for 16 hours. Membranes were washed at 42°C, twice with 2x standard saline phosphate [0.18 mol/L NaCl/10 mmol/L phosphate (pH 7.4)], 1 mmol/L EDTA (saline-sodium phosphate-EDTA, SSPE), and 0.1% SDS and twice with 0.5x SSPE/0.1% SDS. The oligonucleotides used as probes are the complementary sequences of the mature miRNA (miR Registry):8 miR21 5'-TCAACATCAGTCTGATAAGCTA-3'; miR125b1: 5'-TCACAAGTTAGGGTCTCAGGGA-3'; miR145: 5'-AAGGGATTCCTGGGAAAACTGGAC-3'. An oligonucleotide complementary to the U6 RNA (5'-GCAGGGGCCATGCTAATCTTCTCTGTATCG-3') was used to normalize expression levels. Two hundred nanograms of each probe was end labeled with 100 mCi [
-32P]ATP using the polynucleotide kinase (Roche, Basel, Switzerland). Blots were stripped in boiling 0.1% SDS for 10 minutes before rehybridization.
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Results |
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To identify miRNA whose expression was significantly different between normal and tumor samples and could identify the different nature of these breast tissues, we made use of ANOVA and class prediction statistical tools.
To identify differentially expressed miRNAs among all the human miRNAs spotted on the chip, the ANOVA analysis on normalized data generated a list of differentially expressed miRNAs (at P < 0.05) between normal breasts and breast cancers (Table 1). Cluster analysis, based on differentially expressed miRNA, generated a tree with clear distinction between normal and cancer tissues (Fig. 1A).
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Given that biological significance of miRNA deregulation relies on their protein-coding gene targets, we analyzed the predicted targets of the most significantly down-regulated and up-regulated miRNAs: miR-10b, miR125b, miR-145, miR-21, and miR-155. The analysis was done using the three algorithms, miRanda, TargetScan, and PicTar, commonly used to predict human miRNA gene targets (20–22). Because any of the three approaches generates an unpredictable number of false positives, results were intersected to identify the genes commonly predicted by at least two of the methods. Results are shown in Supplementary Table S1.
Biopathologic features and microRNA expression. We analyzed results from miRNA expression profiles in breast cancer to evaluate whether a correlation existed with various biopathologic features associated with tumor specimens. We analyzed lobular versus ductal histotypes, breast cancers with differential estrogen receptor or progesterone receptor expression, lymph nodes metastasis, vascular invasion, proliferation index, expression of ERBB2, and immunohistochemical detection of p53. Lobular versus ductal and ERBB2 expression classes did not reveal any differentially expressed miRNA, whereas all other comparisons revealed a small number of differentially expressed miRNAs (P < 0.05). Tumor grade was not analyzed because the only two grade 1 samples were a size too small to be compared with a large number of grade 2 or 3 samples. Complete results are shown in Table 3.
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Discussion |
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Among the differentially expressed miRNAs, miR-10b, miR-125b, miR145, miR-21, and miR-155 emerged as the most consistently deregulated in breast cancer. Three of them, miR-10b, miR-125b, and miR-145, were down-regulated and the remaining two, miR-21 and miR-155, were up-regulated, suggesting that they may potentially act as tumor suppressor genes or oncogenes, respectively.
It has been reported that the miR-125b, a putative homologue of lin-4 in Caenorhabditis elegans, and the let-7 miRNAs are induced during in vitro retinoic acid–induced differentiation of Tera-2 or embryonic stem cells. Furthermore, high expression of human miR-125b seems to be present in differentiated cells or tissues (23). Here, we show that breast cancer primary tumors and cell lines show evidence of a decreased level of miR-125b expression, suggesting that lack of miR-125 may impair differentiation capabilities of cancer cells.
At present, the lack of knowledge about bona fide miRNA gene targets hampers a full understanding on the biological functions deregulated by miRNA aberrant expression. To partially overcome this limitation, we made use of presently available computational approaches to predict gene targets (21, 22, 24). Supplementary Table S1 shows targets that were predicted by at least two of the methods, and shows that various cancer-associated genes are potentially regulated by miRNAs aberrantly expressed in breast cancer.
It may be expected that targets of down-regulated miRNAs include oncogenes or genes encoding proteins with potential oncogenic functions. Indeed, among putative targets, several genes with potential oncogenic functions could be found, such as FLT1 and the v-crk homologue, the growth factor BDNF, and the transducing factor SHC1 predicted as miR-10b targets. Among putative targets of miR-125b, potential oncogenic functions included the oncogenes YES, ETS1, TEL, and AKT3; the growth factor receptor FGFR2; or members of the mitogen-activated signal transduction pathway VTS58635, MAP3K10, MAP3K11, and MAPK14. The oncogenes MYCN, FOS, YES, and FLI1; integration site of Friend leukemia virus; cell cycle promoters such as cyclins D2 and L1; and MAPK transduction proteins such as MAP3K3 and MAP4K4 were predicted targets for miR-145. Interestingly, the proto-oncogene YES and the core-binding transcription factor CBFB were potential targets of both miR-125 and miR-145.
For the up-regulated miRNAs miR-21 and miR-155, it may be expected that gene targets belong to the class of tumor suppressor genes. For miR-21, the TGFB gene was predicted as target of miR-21 by all three methods. For miR-155, potential targets included the tumor suppressor genes SOCS1 and APC, and the kinase WEE1, which blocks the activity of Cdc2 and prevents entry into mitosis. The hypoxia-inducible factor HIF1A was also a predicted target. Interestingly, among predicted genes, the tripartite motif-containing protein TRIM2, the proto-oncogene SKI, and the RAS homologues RAB6A and RAB6C were found as potential targets of both miR-21 and miR-155.
miRNAs were found differentially expressed in various biopathologic features distinctive of human breast cancer. Some of these findings are worth noticing. For example, mir-30s are all down-regulated in both estrogen receptor– and progesterone receptor–negative tumors, suggesting that expression of these miRNAs is regulated by these hormones. Another interesting observation is the finding that the expression of various let-7 miRNAs was down-regulated in breast cancer samples with either lymph node metastasis or higher proliferation index, suggesting that a reduced let-7 expression could be associated with a poor prognosis. An association between let-7 down-regulation and poor prognosis was previously reported in human lung cancer (6). The finding that the let-7 family of miRNAs regulates the expression of the RAS oncogene family provides a potential explanation for the role of the let-7 miRNAs in human cancer (25). Two miRNA, miR-145 and miR-21, whose expression could differentiate cancer versus normal tissues, were also differentially expressed in cancers with different proliferation indexes or different tumor stage. In particular, miR-145 is progressively down-regulated from normal breast to cancer with high proliferation index. Similarly, but in opposite direction, miR-21 is progressively up-regulated from normal breast to cancers with high tumor stage. These findings suggest that deregulation of these two miRNAs may affect critical molecular events involved in tumor progression. Another miRNA potentially involved in cancer progression is miR-9-3. miR-9-3 was down-regulated in breast cancers with either high vascular invasion or presence of lymph node metastasis, suggesting that its down-regulation was acquired in the course of tumor progression and, in particular, during the acquisition of cancer metastatic potential.
It has been reported that miRNA genes are frequently located in chromosomal regions characterized by nonrandom aberrations in human cancer, suggesting that resident miRNA expression might be affected by these genetic abnormalities (9). miR-125b, which is down-modulated in breast cancer, is located at chromosome 11q23-24, one of the regions most frequently deleted in breast, ovarian, and lung tumors (26, 27). The recognition of a bona fide tumor suppressor gene located at 11q23-24 involved in the pathogenesis of human breast cancer is still lacking. The miR-125b gene establishes itself as an important candidate for this role.
Results reported here increase our understanding of the molecular basis of human breast cancer and suggest that aberrant expression of miRNA genes may be important for the pathogenesis of this human neoplasm.
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Acknowledgments |
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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Footnotes |
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M.V. Iorio and M. Ferracine contributed equally to this work. R. Spizzo is a recipient of an Associazione Italiana per la Ricerca sul Cancro fellowship.
7 http://www-stat.stanford.edu/~tibs/PAM/index.html. 
8 http://www.sanger.ac.uk/Software/Rfam/mirna/.
9 http://www-stat.stanford.edu/~tibs/.
Received 5/23/05. Revised 6/22/05. Accepted 6/24/05.
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 L.-X. Yan, X.-F. Huang, Q. Shao, M.-Y. Huang, L. Deng, Q.-L. Wu, Y.-X. Zeng, and J.-Y. Shao MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis RNA, November 1, 2008; 14(11): 2348 - 2360. [Abstract] [Full Text] [PDF]
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T. E. Miller, K. Ghoshal, B. Ramaswamy, S. Roy, J. Datta, C. L. Shapiro, S. Jacob, and S. Majumder MicroRNA-221/222 Confers Tamoxifen Resistance in Breast Cancer by Targeting p27Kip1 J. Biol. Chem., October 31, 2008; 283(44): 29897 - 29903. [Abstract] [Full Text] [PDF]
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S. D. N. Reddy, K. Ohshiro, S. K. Rayala, and R. Kumar MicroRNA-7, a Homeobox D10 Target, Inhibits p21-Activated Kinase 1 and Regulates Its Functions Cancer Res., October 15, 2008; 68(20): 8195 - 8200. [Abstract] [Full Text] [PDF]
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L. J. Chin, E. Ratner, S. Leng, R. Zhai, S. Nallur, I. Babar, R.-U. Muller, E. Straka, L. Su, E. A. Burki, et al. A SNP in a let-7 microRNA Complementary Site in the KRAS 3' Untranslated Region Increases Non-Small Cell Lung Cancer Risk Cancer Res., October 15, 2008; 68(20): 8535 - 8540. [Abstract] [Full Text] [PDF]
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T. Papagiannakopoulos, A. Shapiro, and K. S. Kosik MicroRNA-21 Targets a Network of Key Tumor-Suppressive Pathways in Glioblastoma Cells Cancer Res., October 1, 2008; 68(19): 8164 - 8172. [Abstract] [Full Text] [PDF]
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A. Markou, E. G. Tsaroucha, L. Kaklamanis, M. Fotinou, V. Georgoulias, and E. S. Lianidou Prognostic Value of Mature MicroRNA-21 and MicroRNA-205 Overexpression in Non-Small Cell Lung Cancer by Quantitative Real-Time RT-PCR Clin. Chem., October 1, 2008; 54(10): 1696 - 1704. [Abstract] [Full Text] [PDF]
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M. Yamakuchi, M. Ferlito, and C. J. Lowenstein miR-34a repression of SIRT1 regulates apoptosis PNAS, September 9, 2008; 105(36): 13421 - 13426. [Abstract] [Full Text] [PDF]
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J. A. Foekens, A. M. Sieuwerts, M. Smid, M. P. Look, V. de Weerd, A. W. M. Boersma, J. G. M. Klijn, E. A. C. Wiemer, and J. W. M. Martens Four miRNAs associated with aggressiveness of lymph node-negative, estrogen receptor-positive human breast cancer PNAS, September 2, 2008; 105(35): 13021 - 13026. [Abstract] [Full Text] [PDF]
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 W. Tam The Emergent Role of MicroRNAs in Molecular Diagnostics of Cancer J. Mol. Diagn., September 1, 2008; 10(5): 411 - 414. [Abstract] [Full Text] [PDF]
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S. Ambs, R. L. Prueitt, M. Yi, R. S. Hudson, T. M. Howe, F. Petrocca, T. A. Wallace, C.-G. Liu, S. Volinia, G. A. Calin, et al. Genomic Profiling of MicroRNA and Messenger RNA Reveals Deregulated MicroRNA Expression in Prostate Cancer Cancer Res., August 1, 2008; 68(15): 6162 - 6170. [Abstract] [Full Text] [PDF]
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N. Kondo, T. Toyama, H. Sugiura, Y. Fujii, and H. Yamashita miR-206 Expression Is Down-regulated in Estrogen Receptor {alpha}-Positive Human Breast Cancer Cancer Res., July 1, 2008; 68(13): 5004 - 5008. [Abstract] [Full Text] [PDF]
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K. Nie, M. Gomez, P. Landgraf, J.-F. Garcia, Y. Liu, L. H.C. Tan, A. Chadburn, T. Tuschl, D. M. Knowles, and W. Tam MicroRNA-Mediated Down-Regulation of PRDM1/Blimp-1 in Hodgkin/Reed-Sternberg Cells: A Potential Pathogenetic Lesion in Hodgkin Lymphomas Am. J. Pathol., July 1, 2008; 173(1): 242 - 252. [Abstract] [Full Text] [PDF]
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O. Kovalchuk, J. Filkowski, J. Meservy, Y. Ilnytskyy, V. P. Tryndyak, V. F. Chekhun, and I. P. Pogribny Involvement of microRNA-451 in resistance of the MCF-7 breast cancer cells to chemotherapeutic drug doxorubicin Mol. Cancer Ther., July 1, 2008; 7(7): 2152 - 2159. [Abstract] [Full Text] [PDF]
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 K. Chen, F. Song, G. A. Calin, Q. Wei, X. Hao, and W. Zhang Polymorphisms in microRNA targets: a gold mine for molecular epidemiology Carcinogenesis, July 1, 2008; 29(7): 1306 - 1311. [Abstract] [Full Text] [PDF]
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A. Brendle, H. Lei, A. Brandt, R. Johansson, K. Enquist, R. Henriksson, K. Hemminki, P. Lenner, and A. Forsti Polymorphisms in predicted microRNA-binding sites in integrin genes and breast cancer: ITGB4 as prognostic marker Carcinogenesis, July 1, 2008; 29(7): 1394 - 1399. [Abstract] [Full Text] [PDF]
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S. Kim, U. J. Lee, M. N. Kim, E.-J. Lee, J. Y. Kim, M. Y. Lee, S. Choung, Y. J. Kim, and Y.-C. Choi MicroRNA miR-199a* Regulates the MET Proto-oncogene and the Downstream Extracellular Signal-regulated Kinase 2 (ERK2) J. Biol. Chem., June 27, 2008; 283(26): 18158 - 18166. [Abstract] [Full Text] [PDF]
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 Q. Yin, J. McBride, C. Fewell, M. Lacey, X. Wang, Z. Lin, J. Cameron, and E. K. Flemington MicroRNA-155 Is an Epstein-Barr Virus-Induced Gene That Modulates Epstein-Barr Virus-Regulated Gene Expression Pathways J. Virol., June 1, 2008; 82(11): 5295 - 5306. [Abstract] [Full Text] [PDF]
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 A. Hudder and R. F. Novak miRNAs: Effectors of Environmental Influences on Gene Expression and Disease Toxicol. Sci., June 1, 2008; 103(2): 228 - 240. [Abstract] [Full Text] [PDF]
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M. Jongen-Lavrencic, S. M. Sun, M. K. Dijkstra, P. J. M. Valk, and B. Lowenberg MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia Blood, May 15, 2008; 111(10): 5078 - 5085. [Abstract] [Full Text] [PDF]
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M. N. Nikiforova, G. C. Tseng, D. Steward, D. Diorio, and Y. E. Nikiforov MicroRNA Expression Profiling of Thyroid Tumors: Biological Significance and Diagnostic Utility J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1600 - 1608. [Abstract] [Full Text] [PDF]
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J.-W. Lee, C. H. Choi, J.-J. Choi, Y.-A. Park, S.-J. Kim, S. Y. Hwang, W. Y. Kim, T.-J. Kim, J.-H. Lee, B.-G. Kim, et al. Altered MicroRNA Expression in Cervical Carcinomas Clin. Cancer Res., May 1, 2008; 14(9): 2535 - 2542. [Abstract] [Full Text] [PDF]
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E. J. Nam, H. Yoon, S. W. Kim, H. Kim, Y. T. Kim, J. H. Kim, J. W. Kim, and S. Kim MicroRNA Expression Profiles in Serous Ovarian Carcinoma Clin. Cancer Res., May 1, 2008; 14(9): 2690 - 2695. [Abstract] [Full Text] [PDF]
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S. Sengupta, J. A. den Boon, I-H. Chen, M. A. Newton, S. A. Stanhope, Y.-J. Cheng, C.-J. Chen, A. Hildesheim, B. Sugden, and P. Ahlquist MicroRNA 29c is down-regulated in nasopharyngeal carcinomas, up-regulating mRNAs encoding extracellular matrix proteins PNAS, April 15, 2008; 105(15): 5874 - 5878. [Abstract] [Full Text] [PDF]
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 G. A. Calin and C. M. Croce MicroRNA-Cancer Connection: The Beginning of a New Tale Am. Assoc. Cancer Res. Educ. Book, April 12, 2008; 2008(1): 667 - 675. [Abstract] [Full Text] [PDF]
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K.-i. Kozaki, I. Imoto, S. Mogi, K. Omura, and J. Inazawa Exploration of Tumor-Suppressive MicroRNAs Silenced by DNA Hypermethylation in Oral Cancer Cancer Res., April 1, 2008; 68(7): 2094 - 2105. [Abstract] [Full Text] [PDF]
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 A. Cohen, M. Shmoish, L. Levi, U. Cheruti, B. Levavi-Sivan, and E. Lubzens Alterations in Micro-Ribonucleic Acid Expression Profiles Reveal a Novel Pathway for Estrogen Regulation Endocrinology, April 1, 2008; 149(4): 1687 - 1696. [Abstract] [Full Text] [PDF]
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 C. Zhang MicroRNomics: a newly emerging approach for disease biology Physiol Genomics, April 1, 2008; 33(2): 139 - 147. [Abstract] [Full Text] [PDF]
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D. Landi, F. Gemignani, A. Naccarati, B. Pardini, P. Vodicka, L. Vodickova, J. Novotny, A. Forsti, K. Hemminki, F. Canzian, et al. Polymorphisms within micro-RNA-binding sites and risk of sporadic colorectal cancer Carcinogenesis, March 1, 2008; 29(3): 579 - 584. [Abstract] [Full Text] [PDF]
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C. Camps, F. M. Buffa, S. Colella, J. Moore, C. Sotiriou, H. Sheldon, A. L. Harris, J. M. Gleadle, and J. Ragoussis hsa-miR-210 Is Induced by Hypoxia and Is an Independent Prognostic Factor in Breast Cancer Clin. Cancer Res., March 1, 2008; 14(5): 1340 - 1348. [Abstract] [Full Text] [PDF]
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 A. Feber, L. Xi, J. D. Luketich, A. Pennathur, R. J. Landreneau, M. Wu, S. J. Swanson, T. E. Godfrey, and V. R. Litle MicroRNA expression profiles of esophageal cancer. J. Thorac. Cardiovasc. Surg., February 1, 2008; 135(2): 255 - 260. [Abstract] [Full Text] [PDF]
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Q. Yin, X. Wang, J. McBride, C. Fewell, and E. Flemington B-cell Receptor Activation Induces BIC/miR-155 Expression through a Conserved AP-1 Element J. Biol. Chem., February 1, 2008; 283(5): 2654 - 2662. [Abstract] [Full Text] [PDF]
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 A. J. Schetter, S. Y. Leung, J. J. Sohn, K. A. Zanetti, E. D. Bowman, N. Yanaihara, S. T. Yuen, T. L. Chan, D. L. W. Kwong, G. K. H. Au, et al. MicroRNA Expression Profiles Associated With Prognosis and Therapeutic Outcome in Colon Adenocarcinoma JAMA, January 30, 2008; 299(4): 425 - 436. [Abstract] [Full Text] [PDF]
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H. Yang, W. Kong, L. He, J.-J. Zhao, J. D. O'Donnell, J. Wang, R. M. Wenham, D. Coppola, P. A. Kruk, S. V. Nicosia, et al. MicroRNA Expression Profiling in Human Ovarian Cancer: miR-214 Induces Cell Survival and Cisplatin Resistance by Targeting PTEN Cancer Res., January 15, 2008; 68(2): 425 - 433. [Abstract] [Full Text] [PDF]
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A. J. Lowery, N. Miller, R. E. McNeill, and M. J. Kerin MicroRNAs as Prognostic Indicators and Therapeutic Targets: Potential Effect on Breast Cancer Management Clin. Cancer Res., January 15, 2008; 14(2): 360 - 365. [Abstract] [Full Text] [PDF]
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J. Jiang, Y. Gusev, I. Aderca, T. A. Mettler, D. M. Nagorney, D. J. Brackett, L. R. Roberts, and T. D. Schmittgen Association of MicroRNA Expression in Hepatocellular Carcinomas with Hepatitis Infection, Cirrhosis, and Patient Survival Clin. Cancer Res., January 15, 2008; 14(2): 419 - 427. [Abstract] [Full Text] [PDF]
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L. B. Frankel, N. R. Christoffersen, A. Jacobsen, M. Lindow, A. Krogh, and A. H. Lund Programmed Cell Death 4 (PDCD4) Is an Important Functional Target of the MicroRNA miR-21 in Breast Cancer Cells J. Biol. Chem., January 11, 2008; 283(2): 1026 - 1033. [Abstract] [Full Text] [PDF]
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P. E. Blower, J.-H. Chung, J. S. Verducci, S. Lin, J.-K. Park, Z. Dai, C.-G. Liu, T. D. Schmittgen, W. C. Reinhold, C. M. Croce, et al. MicroRNAs modulate the chemosensitivity of tumor cells Mol. Cancer Ther., January 1, 2008; 7(1): 1 - 9. [Abstract] [Full Text] [PDF]
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L. F. Sempere, M. Christensen, A. Silahtaroglu, M. Bak, C. V. Heath, G. Schwartz, W. Wells, S. Kauppinen, and C. N. Cole Altered MicroRNA Expression Confined to Specific Epithelial Cell Subpopulations in Breast Cancer Cancer Res., December 15, 2007; 67(24): 11612 - 11620. [Abstract] [Full Text] [PDF]
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X.-B. Shi, L. Xue, J. Yang, A.-H. Ma, J. Zhao, M. Xu, C. G. Tepper, C. P. Evans, H.-J. Kung, and R. W. deVere White An androgen-regulated miRNA suppresses Bak1 expression and induces androgen-independent growth of prostate cancer cells PNAS, December 11, 2007; 104(50): 19983 - 19988. [Abstract] [Full Text] [PDF]
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R. L. Skalsky, M. A. Samols, K. B. Plaisance, I. W. Boss, A. Riva, M. C. Lopez, H. V. Baker, and R. Renne Kaposi's Sarcoma-Associated Herpesvirus Encodes an Ortholog of miR-155 J. Virol., December 1, 2007; 81(23): 12836 - 12845. [Abstract] [Full Text] [PDF]
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B. Shi, L. Sepp-Lorenzino, M. Prisco, P. Linsley, T. deAngelis, and R. Baserga Micro RNA 145 Targets the Insulin Receptor Substrate-1 and Inhibits the Growth of Colon Cancer Cells J. Biol. Chem., November 9, 2007; 282(45): 32582 - 32590. [Abstract] [Full Text] [PDF]
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L. Lu, D. Katsaros, I. A. Rigault de la Longrais, O. Sochirca, and H. Yu Hypermethylation of let-7a-3 in Epithelial Ovarian Cancer Is Associated with Low Insulin-like Growth Factor-II Expression and Favorable Prognosis Cancer Res., November 1, 2007; 67(21): 10117 - 10122. [Abstract] [Full Text] [PDF]
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H. A. Meijer, M. Bushell, K. Hill, T. W. Gant, A. E. Willis, P. Jones, and C. H. de Moor A novel method for poly(A) fractionation reveals a large population of mRNAs with a short poly(A) tail in mammalian cells Nucleic Acids Res., October 11, 2007; (2007) gkm830v1. [Abstract] [Full Text] [PDF]
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M. Gironella, M. Seux, M.-J. Xie, C. Cano, R. Tomasini, J. Gommeaux, S. Garcia, J. Nowak, M. L. Yeung, K.-T. Jeang, et al. Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development PNAS, October 9, 2007; 104(41): 16170 - 16175. [Abstract] [Full Text] [PDF]
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X. Tang, J. Gal, X. Zhuang, W. Wang, H. Zhu, and G. Tang A simple array platform for microRNA analysis and its application in mouse tissues RNA, October 1, 2007; 13(10): 1803 - 1822. [Abstract] [Full Text] [PDF]
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M. V. Iorio, R. Visone, G. Di Leva, V. Donati, F. Petrocca, P. Casalini, C. Taccioli, S. Volinia, C.-G. Liu, H. Alder, et al. MicroRNA Signatures in Human Ovarian Cancer Cancer Res., September 15, 2007; 67(18): 8699 - 8707. [Abstract] [Full Text] [PDF]
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B. Berkhout and K.-T. Jeang RISCy Business: MicroRNAs, Pathogenesis, and Viruses J. Biol. Chem., September 14, 2007; 282(37): 26641 - 26645. [Full Text] [PDF]
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M. Kruhoffer, L. Dyrskjot, T. Voss, R. L.P. Lindberg, R. Wyrich, T. Thykjaer, and T. F. Orntoft Isolation of Microarray-Grade Total RNA, MicroRNA, and DNA from a Single PAXgene Blood RNA Tube J. Mol. Diagn., September 1, 2007; 9(4): 452 - 458. [Abstract] [Full Text] [PDF]
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W. Zhang, J. E. Dahlberg, and W. Tam MicroRNAs in Tumorigenesis: A Primer Am. J. Pathol., September 1, 2007; 171(3): 728 - 738. [Abstract] [Full Text] [PDF]
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C. D. Johnson, A. Esquela-Kerscher, G. Stefani, M. Byrom, K. Kelnar, D. Ovcharenko, M. Wilson, X. Wang, J. Shelton, J. Shingara, et al. The let-7 MicroRNA Represses Cell Proliferation Pathways in Human Cells Cancer Res., August 15, 2007; 67(16): 7713 - 7722. [Abstract] [Full Text] [PDF]
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D. Loffler, K. Brocke-Heidrich, G. Pfeifer, C. Stocsits, J. Hackermuller, A. K. Kretzschmar, R. Burger, M. Gramatzki, C. Blumert, K. Bauer, et al. Interleukin-6 dependent survival of multiple myeloma cells involves the Stat3-mediated induction of microRNA-21 through a highly conserved enhancer Blood, August 15, 2007; 110(4): 1330 - 1333. [Abstract] [Full Text] [PDF]
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S. Galardi, N. Mercatelli, E. Giorda, S. Massalini, G. V. Frajese, S. A. Ciafre, and M. G. Farace miR-221 and miR-222 Expression Affects the Proliferation Potential of Human Prostate Carcinoma Cell Lines by Targeting p27Kip1 J. Biol. Chem., August 10, 2007; 282(32): 23716 - 23724. [Abstract] [Full Text] [PDF]
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 A. Goga and C. Benz Anti-Oncomir Suppression of Tumor Phenotypes Mol. Interv., August 1, 2007; 7(4): 199 - 202. [Abstract] [Full Text] [PDF]
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