Long noncoding RNA UCA1 promotes autophagy by targeting miR-96-5p in acute myeloid leukemia.

Long noncoding RNA UCA1 promotes autophagy by targeting miR-96-5p in acute myeloid leukemia. Clin Exp Pharmacol Physiol. 2020 Jan 17;: Authors: Li JJ, Chen XF, Wang M, Zhang PP, Zhang F, Zhang JJ Abstract Long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been identified as an oncogene and is involved in acute myeloid leukemia (AML). Autophagy contributes to tumorigenesis and cancer cell survival. The purpose of this study was to investigate the regulatory role and mechanism of UCA1 in AML cell viability by its effect on autophagy. The expression of UCA1, miR-96-5p, and ATG7 was determined by qRT-PCR and western blot. Cell proliferation was examined by MTT assay. The autophagy level was assessed by green fluorescent protein (GFP)-LC3 immunofluorescence and western blot. The interaction between UCA1 and miR-96-5p or ATG7 was analyzed by luciferase reporter activity. The results showed that UCA1 promoted AML cell proliferation by inducing autophagy. Mechanistically, UCA1 acted as a sponge of miR-96-5p by binding to miR-96-5p. ATG7 was a direct target of miR-96-5p and positively regulated by UCA1. Further results showed that the miR-96-5p mimic effectively counteracted the UCA1 overexpression-mediated induction of the ATG7/autophagy pathway. Collectively, UCA1 functions as a sponge of miR-96-5p to upregulate its target ATG7, thereby resulting in autophagy induction. Our findings reveal a UCA1-mediated molecular mec...
Source: Clinical and Experimental Pharmacology and Physiology - Category: Drugs & Pharmacology Authors: Tags: Clin Exp Pharmacol Physiol Source Type: research