| miR-222 expression was significantly reduced in prostate cancer tissues, suggesting that miR-222 may act as tumor suppressor | prostate, |
| R-221/222 can be regarded as a new family of oncogenes, directly targeting the tumor suppressor p27(Kip1), and their overexpression might be contribute to the oncogenesis and progression of prostate carcinoma through p27(Kip1) down-regulation | prostate, |
| miR-221 and miR-222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1. | prostate, |
| The inhibition of the highly expressed miR-221 and miR-222 impairs the growth of prostate carcinoma xenografts in mice. | prostate, |
| Functional links between clustered microRNAs: suppression of cell-cycle inhibitors by microRNA clusters in gastric cancer. | gastric, |
| study provides the first evidence for an oncogenic activity of miR-155, miR-203, miR-210 and miR-222 in the development of pancreatic cancer as has been reported for other tumor types | pancreatic, |
| High-mobility group A1 proteins enhance the expression of the oncogenic miR-222 in lung cancer cells. | lung, |
| miR-221/222 function as oncogenic microRNAs in human gliomas, at least in part, by targeting Cx43. | glioma, |
| Increased miR-222 in H. pylori-associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK. | gastric, |
| overexpression of oncogenic miR-221 and miR-222 caused by HMGB1 is associated with an increase in malignancy scores of papillary thyroid cancer cells, namely cell growth and motility | thyroid, |
| Overexpression of primary microRNA 221/222 in acute myeloid leukemia. | leukemia, |
| miR-221/222 represents a novel molecular marker and putative oncogene in acute myeloid leukemia | leukemia, |
| Data indicate that overexpressed miR-221/222 may play an oncogenic role in pancreatic cancer by inducing the expression of MMP-2 and MMP-9, thus leading to cancer cell invasion. | pancreatic, |
| miR-221&222 regulate TRAIL resistance and enhance tumorigenicity through PTEN and TIMP3 downregulation. | None |
| results suggest that miR-221/222 overexpression might be one of the factors contributing to oncogenesis and progression of atypical teratoid-rhabdoid tumors through p27Kip1 downregulation | None |