HIGHLIGHTS
SUMMARY
The authors found that miR-17-5p promoted 5-FU resistance in CRC in_vitro and in_vivo; specifically, miR-17-5p enhanced mitochondrial fission and mitophagy, thereby regulating mitochondrial function and leading to 5-FU resistance. miR-175p upregulation is attributable to m6A modification mediated by METTL14 and YTHDC2, which leads to reduced degradation of primiR-17. To construct cell lines overexpressing exogenous miR-17-5p, full-length hsa-miR-17-5p (GeneChem, China) and the empty control were cloned into the lentiviral_vector system (puro-miR-17-5p and puro-NC). METTL14 depletion significantly enhances . . .
If you want to have access to all the content you need to log in!
Thanks :)
If you don't have an account, you can create one here.