Long noncoding RNA HAGLROS promotes cell proliferation, inhibits apoptosis and enhances autophagy via regulating miR-5095/ATG12 axis in hepatocellular carcinoma cells.

In this research, we planned to dig the possible influences and mechanism of long noncoding (lnc) RNA HAGLROS in the development and progression of hepatocellular carcinoma (HCC). The levels of lncRNA HAGLROS in HCC tumor samples and their relationship with clinicopathological characteristics and prognosis of patients with HCC were studied. Subsequently, overexpression and silenced approaches were used in HCC cells for detecting the effects of lncRNA HAGLROS on cell viability, apoptosis, and autophagy. Furthermore, we investigated whether HAGLROS could function as a competing endogenous RNA (ceRNA) to regulate miR-5095 expression in HCC cells, and explored the correlation between miR-5095 and ATG12. Besides, the correlation of HAGLROS, the consequent PI3K/AKT/mTOR signaling pathway was further explored. The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation. In contrast to the lower level, a higher level of HAGLROS correlated with a shorter survival time of patients with HCC. The suppression of HAGLROS decreased cell viability, promoted apoptosis, and inhibited autophagy. Moreover, HAGLROS negatively regulated miR-5095 expression, which further regulated HCC cell viability, apoptosis, and autophagy. In addition, ATG12 was targeted by miR-5095 and was then involved in miR-5095-regulated HCC cell biological processes including viability, apoptosis, and autophagy. Furthermore, overexpression of HAGLROS activated PI3K/AKT/mTOR signals. Our results revealed that HAGLROS is highly expressed in HCC, and its high level may correlate with the progression and development of HCC involving the processes of cell viability, apoptosis, and autophagy through the miR-5095/ATG12 axis and PI3K/AKT/mTOR signals.