From: Protein glycosylation in cancers and its potential therapeutic applications in neuroblastoma
miRNAs | Glycogene targets | Comments |
---|---|---|
miR-30b/30d | GALNT1, GALNT7 | Both GALNT1 and GALNT7 are targets of miR-30b/d, which are associated with metastasis in melanoma [112]. |
miR-378 | GALNT7 | GALNT7 is a target of miR-378 and plays a critical role in osteoblast differentiation [111]. |
miR-122 | GALNT10, FUT8 | GALNT10 modulates O-glycosylation of EGFR in hepatitis B virus (HBV)-infected hepatoma cells. GALNT10 is a target of miR-122, whose gene transcription is activated by hepatocyte nuclear factor 4α (Hnf4α). Therefore, a regulatory pathway of Hnf4α/miR-122/GALNT10/EGFR may develop as therapeutic targets [113]. Ectopic expression of miR-122 can significantly decrease FUT8 levels, thus may play a role in the dysregulation of core fucosylation observed in liver tumors [114]. |
miR-27a | B4GALT3 | B4GALT3 up-regulated by miR-27a contributes to the tumorigenic activities by β1-integrin pathway and might provide potential biomarkers for cervical cancer [117]. |
miR-148b | C1GALT1 | Inhibition of miR-148b expression can reverse the lower levels of C1GALT1 typical of IgA nephropathy. Therefore, miR-148b levels may be manipulated to provide a therapeutic approach to the disease [110]. |
miR-199b-5p | FUT4 | The cluster of differentiation carbohydrate antigen CD15, also known as FUT4, is a marker of medulloblastoma tumor-propagating cells and an additional direct target of miR-199b-5p. Therefore, the finely tuned regulation of miR-199b-5p may have a role in therapeutic application in medulloblastoma [115]. |
miR-34a | FUT8 | Ectopic expression of miR-34a can significantly decrease FUT8 levels, thus may play a role in the dysregulation of core fucosylation observed in liver tumors [114]. |
miR-125b | ERManI | ERManI functions as a “gate keeper” in the Golgi complex to facilitate the retention and recycling of misfolded glycoproteins escaped from the ER. In hepatoma cells, however, ERManI regulates transformation phenotypes independent of ER-stress. ERManI knockdown by miR-125b inhibits proliferation and migration of hepatoma cells [116]. |