| MiR-25 may function as a tumor suppressor by targeting Smad7 in colon cancer. | colorectal, |
| SOX4 overexpression rescued miR-25-induced suppression of proliferation, migration, and invasion of osteosarcoma cells. Taken together, these results suggest that miR-25 functions as a tumor suppressor in the progression of osteosarcoma by repressing SOX4. | osteosarcoma, |
| miRNA253p may act as a tumor suppressor by targeting SOX4 expression in bone tissue. | None |
| Our study shows miR-25 is overexpressed in small cell lung cancer and acting as oncogenic regulator by regulating cyclin E2. | lung, |
| we observed Dickkopf-related protein 3 (DKK3) as a direct target of miR-25 in vitro. Upregulation of DKK3 partially attenuated the oncogenic effect of miR-25 on melanoma cells. Ectopic expression of miR-25 in melanoma cells induced beta-catenin accumulation in nuclear and inhibited TCF4 (T cell factor 4) activity, as well as the expression of c-Myc and Cyclin D1. | skin, |
| These results show that miR-25-3p has intracellular and extracellular oncogenic functions as well as clinicopathological relevance in osteosarcoma, indicating its potential as a novel diagnostic and therapeutic tool for the clinical management of this disease. | osteosarcoma, |
| Study reports the oncogenic role of miR-25-3p in pancreatic cells induced by cigarette smoke condensate (CSC) via the N(6)-methyladenosine (m6A) mechanism. CSC-induced METTL3-miR-25-3p-PHLPP2-AKT axis promotes the initiation and the progression of pancreatic ductal adenocarcinoma. | pancreatic, |
| oncogenic miR-25-3p directly targets BTG2 in TNBC. Further studies revealed that the biological effects of miR-25-3p on TNBC cell proliferation and apoptosis were mediated through regulation of BTG2 and subsequent activation of AKT and ERK-MAPK signaling pathway. | None |