Table 6 Fold change in expression of miRNAs after treatments with cisplatin, etoposide and bleomycin with respect to control. In column 3, ‘↑’ represents significant (P < 0.05) increase; ‘↓’ represents significant (P < 0.05) decrease; and ‘-’ represents non-significant (P>0.05) change
1. BiologicalFunction | 2. miRNA | 3. Significant Fold change (p < 0.5) | 4. Reports from previous studies | 5. Ref. | ||
|---|---|---|---|---|---|---|
Cisplatin | Etoposide | Bleomycin | ||||
Pluripotency | miR-145-3p | No expression | No expression | No expression | Represses OCT4, SOX2, and KLF4 and thus pluripotency in human embryonic stem cells | [34] |
miR-106b-5p | – | 1.8 ↑ | 1.5 ↑ | Promotes Proliferation by targeting B3G, promotes stem-cell-like phenotype | ||
miR-185-5p | – | 1.5 ↑ | 2.4 ↑ | Inhibits cell proliferation and induces cell apoptosis by targeting VEGFA | [37] | |
Cell cycle and proliferation | let-7a-5p | – | 1.4 ↑ | 1.5 ↑ | High expression inhibit proliferation and induce apoptosis | [38] |
miR-34a | 1.7 ↑ | – | 2.1 ↓ | Ectopic miR-34a induced apoptosis and a cell cycle arrest in the G1-phase, by targeting p53 | ||
Apoptosis | miR-17-3p | – | 2.1 ↓ | – | miR-17-3p is downregulated when p53 is active, thus inducing apotosis and vice versa | [40] |
miR-34c-5p | 6.5 ↑ | 6.5↑ | 60.8 ↑ | miR-34c-5p was downregulated in paclitaxel-resistant gastric cancer samples, MiR-34c enhances chemosensitivity of Ishikawa cell to cisplatin | ||
Chemosensitivity | miR-449a | 19.7 ↓ | 27.3 ↓ | 31.6 ↓ | Ectopic expression of miR-449a increased the apoptosis induced by cisplatin, miR-449a is proapoptotic and targets BCL2 expression | |