Long non‐coding RNA UCA1 promotes autophagy by targeting miR‐96‐5p in acute myeloid leukaemia

Abstract

Long non‐coding RNA (lncRNA) urothelial carcinoma‐associated 1 (UCA1) has been identified as an oncogene and is involved in acute myeloid leukaemia (AML). Autophagy contributes to tumourigenesis 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 mechanism responsible for autophagy induction in AML and help to improve the understanding of the molecular mechanism of AML progression.

LncRNA OTUD6B-AS1 promotes paclitaxel resistance in triple negative breast cancer by regulation of miR-26a-5p/MTDH pathway-mediated autophagy and genomic instability

“…In fact, many studies have shown that ncRNA can participate in the regulation of DDR-related genes, and these RNAs are usually also involved in the regulation of autophagy. For example: miR-29 can inhibit autophagy, and can maintain genomic stability by regulating the level of PIK3R1 in breast cancer [ 36 , 37 ]; miR-96 can inhibit autophagy, and can promote the GIN by regulating the level of RAD51 in breast cancer [ 38 , 39 ]; miR-182 can inhibit autophagy by regulating mTOR, and can enhance GIN by regulating BRCA1 in breast cancer [ 40 , 41 ]. It seems that there is heterogeneity in ncRNA regulation of autophagy and GIN.…”

LncRNA UCA1 Promotes the Progression of AML by Upregulating the Expression of CXCR4 and CYP1B1 by Affecting the Stability of METTL14

“…In the previous study, we have demonstrated that UCA1 has been identified as an oncogene and is involved in AML [ 16 ]. In the present study, the CCK8 assay showed that overexpression of UCA1 could promote HL60 and U973 cell proliferation, while suppression of UCA1 inhibited HL60 and U973 cell proliferation ( Figure 1(a) ).…”

MiR-152-5p suppresses osteogenic differentiation of mandible mesenchymal stem cells by regulating ATG14-mediated autophagy

“…We then asked whether miRNA-mediated autophagy played an important role in the development of osteoporosis. To address this question, we selected 10 miRNAs which were associated with autophagy, including miR-20a-5p [ 22 ],miR-125a-5p [ 23 ], miR-146a-5p [ 24 ], miR-378-3p [ 25 ], miR-152-5p [ 26 ], miR-100-5p [ 27 ], miR-140-3p [ 28 ], miR-542-3p [ 29 ], miR-96-5p [ 30 ], miR-185-5p [ 31 ]. QRT-PCR analysis was performed to investigate the differences of these ten miRNAs in MMSC-M of OVX and sham.…”

“…In this study, we constructed mandibular osteoporotic rat model by bilateral ovariectomy and selected ten miRNAs that were reported to regulate autophagy, including miR-20a-5p [ 22 ], miR-125a-5p [ 23 ], miR-146a-5p [ 24 ], miR-378-3p [ 25 ], miR-152-5p [ 26 ], miR-100-5p [ 27 ], miR-140-3p [ 28 ], miR-542-3p [ 29 ], miR-96-5p [ 30 ], miR-185-5p [ 31 ]. We revealed an upregulated miR-152-5p level in maxilla, mandible and MMSCs-M of ovariectomized rats compared with sham group.…”