Long non‑coding RNA LINC01018 inhibits the progression of acute myeloid leukemia by targeting miR‑499a‑5p to regulate PDCD4
- Hong Zhou
- Pengfei Shi
- Xiaofeng Jia
- Qianfu Xue
Affiliations: Department of Hematology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, P.R. China, College of Life Sciences, China Jiliang University, Hangzhou, Zhejiang 310018, P.R. China, Department of Hematology, Yong Chuan Hospital of Chongqing Medical University, Chongqing 402160, P.R. China
- Published online on: May 20, 2021 https://doi.org/10.3892/ol.2021.12802
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Acute myeloid leukemia (AML) is a highly heterogeneous disease with a very high mortality rate. In recent years, an increasing number of studies have proven that long non‑coding RNAs (lncRNAs) and microRNAs (miRNAs) may serve as useful biomarkers in various cancer types. However, the mechanism of LINC01018 and miR‑499a‑5p in AML requires further investigation. The mRNA expression of LINC01018, miR‑499a‑5p and PDCD4 in AML tissues and cells was detected using reverse transcription‑quantitative polymerase chain reaction. Cell proliferation was measured using Cell Counting kit‑8 and EdU assays. Cell apoptosis was monitored via a TUNEL staining assay. Protein expression of PDCD4, Bax and Bcl‑2 was measured using western blot analysis. The interaction between PDCD4 and LINC01018 or miR‑499a‑5p was verified by RNA pull‑down, RIP and dual‑luciferase reporter assays. LINC01018 and PDCD4 were downregulated in AML, while miR‑499a‑5p was upregulated. LINC01018‑overexpression suppressed AML cell proliferation and induced AML cell apoptosis, while miR‑499a‑5p transfection reversed these effects. LINC01018 acted as a sponge of miR‑499a‑5p, and PDCD4 was demonstrated to be targeted by miR‑499a‑5p. Knockdown of miR‑499a‑5p suppressed AML cell proliferation and promoted AML cell apoptosis, but silencing PDCD4 abolished this effect. LINC01018 inhibited AML cell growth by modulating PDCD4 through suppression of miR‑499a‑5p, providing a feasible theoretical basis for the treatment of AML.