ANRIL regulates retinoblastoma progression via targeting autophagy by miR-328-3p/TSC1/ULK signaling.

Abstract

Retinoblastoma is the most common primary intraocular malignancy of childhood. The aim of our study was to investigate the role and regulatory mechanism of the long non-coding RNA ANRIL in retinoblastoma. Here, our data demonstrated that ANRIL overexpression inhibited miR-328-3p expression, but promoted expression of autophagy-related proteins (LC3B, ATG5, and BECN1). Then we predicted the binding sites for ANRIL with miR-328-3p, and for miR-328 3p with TSC1/ULK2 3'-UTR, and confirmed the combination of miR-328-3p and ANRIL and TSC1/ULK2 3'-UTR. Importantly, the data showed that ANRIL overexpression promoted TSC1 and ULK2 expression, and inhibited the phosphorylation of mTOR. Finally, our results indicated that ANRIL overexpression facilitated Y79 cell proliferation and cisplatin-induced apoptosis. Our results indicated that ANRIL promoted the proliferation and cisplatin resistance of Y79 cells through activating autophagy by promoting TSC1/ULK2 ex- pression via acting as a miR-328-3p sponge.