AbstractLong non-coding RNA AK001796 was initially identified altered in lung cancer.
Recent research showed it could participate in the prognosis of hepatocellular
carcinoma (HCC). However, the general biological role of AK001796 and its
underlying mechanisms in HCC remain unclear. Here we demonstrated that the
expression level of AK001796 in HCC tissues and cell lines was up-regulated.
Silencing AK001796 suppressed the proliferation ability of HCC cells. Through
dual luciferase reporter assays and loss/gain of functions studies, we
identified that AK001796 could bind to miR-150, a star microRNA, promoting HCC
proliferation. Furthermore, it was reported that growth factor receptor binding
protein 2-associated binder 1 (GAB1) is a target gene of miR-150. Owing to
AK001796 being a decoy for miR-150 and binding the same putative sites of
miR-150 as GAB1, we presented that inhibition of miR-150 in AK001796 silencing
cells reversed the reduction in GAB1. Subsequently, our findings demonstrated
that silencing AK001796 can impair phospho-ERK1/2 and phospho-AKT. In
conclusion, our investigation revealed that AK001796 promoted proliferation by
enhancing phospho-ERK1/2 and phospho-AKT through AK001796/miR-150/GAB1 axis in
HCC. These results provided further evidence for the critical roles of AK001796
accumulating HCC and suggested that AK001796 might act as an HCC biomarker in
clinical treatment.