AI Article Synopsis
- miRNAs play a critical role in regulating gene expression and show varying levels in diseases like cancer; this study focuses on identifying genes affected by epigenetic changes in prostate cancer.
- After treating prostate cancer cell lines with 5-aza-2'-deoxycytidine and trichostatin A, 38 miRNAs were found to be more active, with six showing lower levels in cancer samples compared to benign cases.
- Notably, the research highlights miR-193b as a potential tumor suppressor, as its activation in specific cancer cells led to reduced cell growth and inhibited anchorage-independent growth.
Article Abstract
miRNAs have proven to be key regulators of gene expression and are differentially expressed in various diseases, including cancer. Our aim was to identify epigenetically dysregulated genes in prostate cancer. We performed miRNA expression profiling after relieving epigenetic modifications in 6 prostate cancer cell lines and nonmalignant prostate epithelial cells. Thirty-eight miRNAs showed increased expression in any prostate cancer cell line after 5-aza-2'-deoxycytidine (5azadC) and trichostatin A (TSA) treatments. Six of these also had decreased expression in clinical prostate cancer samples compared to benign prostatic hyperplasia. Among these, miR-193b was methylated in 22Rv1 cell line at a CpG island approximately 1 kb upstream of the miRNA locus. Expressing miR-193b in 22Rv1 cells using pre-miR-193b oligonucleotides caused a significant growth reduction (p < 0.001) resulting from a decrease of cells in S-phase of the cell cycle (p < 0.01). In addition, the anchorage independent growth was partially inhibited in transiently miR-193b-expressing 22Rv1 cells (p < 0.01). Altogether, our data suggest that miR-193b is an epigenetically silenced putative tumor suppressor in prostate cancer.
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| http://dx.doi.org/10.1002/ijc.25162 | DOI Listing |
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