We generated and monitored liver tumor initiation in Mir122a-null Pten heterozygous (Mir122a<sup>-/-</sup>;Pten<sup>+/-</sup> and Mir122a<sup>-/-</sup>;Alb-Cre;Pten<sup>fx/+</sup>) mice and compared the results with those in Mir122a<sup>-/-</sup> mice.
Lower serum miR-122 is a unique feature of HNF1A-DM patients and might partially explain the increased risk for liver neoplasm and abnormal lipid metabolism in HNF1A-DM patients.
In summary, our results reveal a novel Hnf4α/miR-122/GALNT10 regulatory pathway that facilitates EGF miR-122 activation and hepatoma growth in HBV-associated hepatocarcinogenesis.
Since miR-122 and miR-34a downregulation is a common feature in spontaneous human hepatocarcinoma, our finding that these miRNAs are able to target FUT8 3'UTR suggests that, together with transcriptional and other post-transcriptional systems, a miRNA-mediated mechanism could also be involved in the increased core fucosylation observed in liver tumors.