Genomic profiling of microRNA and mRNA reveals deregulated microRNA expression in prostate cancer

By S. Ambs, R. Prueitt, Ming Yi, R. Hudson, Tiffany M. Howe, F. Petrocca, Tiffany A. Wallace, Chang-Gong Liu, Stefano Volinia, George A. Calin and 3 more. Cancer Research, 2008

705 citations recorded by the source corpus.

MicroRNAs are small non-coding RNAs that regulate the expression of protein-coding genes. To evaluate the involvement of microRNAs in prostate cancer, we determined genome-wide expression of microRNAs and mRNAs in 60 primary prostate tumors and 16 non-tumor prostate tissues. The mRNA analysis revealed that key components of microRNA processing and several microRNA host genes, e.g., MCM7 and C9orf5, were significantly up-regulated in prostate tumors. Consistent with these findings, tumors expressed the miR-106b-25 cluster, which maps to intron 13 of MCM7, and miR-32, which maps to intron 14 of C9orf5, at significantly higher levels than non-tumor prostate. The expression levels of other microRNAs, including a number of miR-106b-25 cluster homologues, were also altered in prostate tumors. Additional differences in microRNA abundance were found between organ-confined tumors and those with extraprostatic disease extension. Lastly, we found evidence that some microRNAs are androgen-regulated and that tumor microRNAs influence transcript abundance of protein-coding target genes in the cancerous prostate. In cell culture, E2F1 and p21/WAF1 were identified as targets of miR-106b, Bim of miR-32, and exportin-6 and protein tyrosine kinase 9 of miR-1. In summary, microRNA expression becomes altered with the development and progression of prostate cancer. Some of these microRNAs regulate the expression of cancer-related genes in prostate cancer cells.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7d1f90ad6c0dd09ad149ae4dbc0648383b9b175b

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Citations in the corpus

microRNAs in cancer (2013, background): “Loss of miR-15a and miR-16-1 has also been observed in prostate cancer and multiple myeloma (106, 107).”
Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “Consistent with these findings, key enzymatic components of miRNA synthesis and processing such as Dicer are up-regulated during prostate tumor progression (Chiosea et al. 2006; Ambs et al. 2008; Poliseno et al. 2010a), while functional analyses of mice with conditional deletion of Dicer support a r”
Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma (2009, background): “For example, the results are based only upon microarray measurements that partially detected pre-miRNAs,15 and the expressions were not validated by RT-PCR.11,15 Furthermore, nonmatching normal tissue from healthy individuals was used, whereas we Table 4.”
MicroRNAs in development and disease. (2011, background): “miRNAs profiling of prostate tumors uncovered the dysregulation of some of the usual culprits, including downregulation of let-7, miR-145, miR-141, miR-125, miR-1, miR-133, miR106b, and miR-16 (12, 466, 491).”
Reprogramming of miRNA networks in cancer and leukemia. (2010, neutral): “GSE8126 and GSE7055 (Ambs et al. 2008), GSE17155 (Fassan et al. 2009), GSE3467 (He et al. 2005), GSE7828 (Schetter et al. 2008), GSE6857 (Budhu et al. 2008), GSE16654 (Chin et al. 2009), and GSE14936 (Seike et al. 2009), and at ArrayExpress (www.ebi.ac.uk/microarray-as/ae) under accession nos.”