Basic—Alimentary TractThe miR-106b-25 Polycistron, Activated by Genomic Amplification, Functions as an Oncogene by Suppressing p21 and Bim
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Materials and Methods
See also Supplementary Materials and Methods for full description.
MiR Microarrays Define Novel EAC-Specific Candidate Tumor-Suppressive miRs and Oncogenic miRs
As a first approach to studying the involvement of miRs in BE-associated neoplasms, we performed miR microarray investigations of nonimmortalized primary normal esophageal (NE) epithelial cells (HEEpiC), BE-derived cell lines (QhTRT, ChTRT, and GihTRT), and an EAC-derived cell line (OE-33). Representative results of these experiments are displayed in Table 1. Several miRs were aberrantly regulated in BE or EAC cells vs NE cells. In particular, we found that miRs-25, -93, and -106b, all of which
Discussion
Although the first miR, lin-4, was discovered in 199318 and the second miR, let-7, in 200019 in Caenorhabditis elegans, only recently has the study of this class of small regulatory RNAs in humans become more widespread.20 Experimental evidence that has accumulated in recent years has led oncologists to speculate that unrevealed molecular actors—particularly noncoding RNAs previously classified as “junk”—play important roles in carcinogenesis. In fact, approximately 70% of the genome has been
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Conflicts of interest The authors disclose no conflicts.
Funding Supported partially by NIH awards CA85069 and CA01808.