| miR-20a plays a role as a tumor suppressor in thyroid cancer cells and targets LIMK1 | thyroid, |
| Differential altered expression of let-7a and miR-205 tumor-suppressor miRNAs in different subtypes of breast cancer under treatment with Taxol | breast, |
| Validation of miR-20a as a Tumor Suppressor Gene in Liver Carcinoma Using Hepatocyte-Specific Hyperactive piggyBac Transposons | liver, |
| Results suggest miR-20a may act as a tumor suppressor in CD4+ T cells and also has a potential therapeutic in these kinds of cancers. | None |
| Oncogenic role of miR-17-92 cluster in anaplastic thyroid cancer cells. | thyroid, |
| Genetic dissection of the miR-17~92 cluster of microRNAs in Myc-induced B-cell lymphomas. | lymphoma, |
| more dedifferentiated prostate cancer cells have a higher expression of miR-20a and this supports the oncogenic role of miR-20a in prostate cancer carcinogenesis | prostate, |
| miR-17~92 cooperates with RB pathway mutations to promote retinoblastoma. | retinoblastoma, |
| miR-20a promotes migration and invasion by regulating TNKS2 in human cervical cancer cells. | cervical, |
| Synthetic lethality between Rb, p53 and Dicer or miR-17-92 in retinal progenitors suppresses retinoblastoma formation. | retinoblastoma, |
| miR-17-5p/20a are important markers for gastric cancer and murine double minute 2 participates in their functional regulation. | gastric, |
| miR-20a-mediated autophagy defect might be a new mechanism underlying the oncogenic function of miRNA during breast tumorigenesis. | breast, |
| MiR20a5p functioned as an oncogene in HNSCC by downregulating TNFRSF21. | HNSC, |
| A microRNA polycistron as a potential human oncogene. | None |
| An E2F/miR-20a autoregulatory feedback loop. | None |
| Overexpression of EGR2 significantly attenuated the oncogenic effect of miR-20a. | None |
| miR20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM. | None |
| miR-19b/20a were oncogenes that may serve critical functions in the pathogenesis of MM by inducing cell proliferation and migration, inhibiting cell apoptosis and altering cell cycle. | None |