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Table 2 Identified glycogene/miRNA interactions in human diseases

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].

  1. B4GALT3 β1,4-galactosyltransferase 3, C1GALT1 core 1 β1,3-galactosyltransferase, FUT fucosyltransferase, GALNT N-acetylgalactosaminyltransferase, ERManI human endoplasmic reticulum alpha-1, 2-mannosidase I