Fig. 10.

The schematic illustrates a model of Long noncoding RNA HULC promotes liver cancer cell growth by inhibition of PTEN via autophagy cooperation to miR15a. HULC decreases mature miR15a and inhibits P62 expression. Furthermore, HULC overexpression increased the expression of LC3I and LC3II (a autophagy marker) dependent on sirt1 (a deacetylase) Notably, HULC enhanced the interplay between LC3 and ATG3.Furthermore, HULC also increased the expression of becline-1(autophagy related gene). Therefore, HULC increased the cellular autophagy by activating sirt1, specifically, under starvation. Furthermore, HULC reduced the expression of PTEN, β-catenin and increased the expression of SAPK/JUNK,PKM2,CDK2, NOTCH1,C-Jun in Hep3B cells. Strikingly, HULC inhibited PTEN through ubiquitin–proteasome system mediated by autophagy-P62. Therefore, HULC activates AKT-PI3K-mTOR pathway via PTEN reduction in liver cancer cells