ArticleFEBS open bio2020
The long non-coding RNA LOC285758 promotes invasion of acute myeloid leukemia cells by down-regulating miR-204-5p.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Long Noncoding RNAs in Progression of Leukemia: Based on Chromosomal Location.MicroRNA (Shariqah, United Arab Emirates) · 2024Review
- NDRG3 regulates imatinib resistance by promoting β‑catenin accumulation in the nucleus in chronic myelogenous leukemia.Oncology reports · 2023Article
- LncRNAIranian journal of public health · 2022Article
- Increased Plasma Levels of lncRNAsCancers · 2021Article
- LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit.Cell death & disease · 2021Article
- Article
- Identification of Acute Myeloid Leukemia Bone Marrow Circulating MicroRNAs.International journal of molecular sciences · 2020Article
- LncRNA ADAMTS9-AS1 Restrains the Aggressive Traits of Breast Carcinoma Cells via Sponging miR-513a-5p.Cancer management and research · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
Acute myeloid leukemia (AML) is the second most common type of leukemia worldwide. It was previously reported that expression of the long noncoding RNA LOC285758 is positively associated with AML cell proliferation, but the underlying mechanisms have not previously been reported. Here, we report that LOC285758 expression is higher in clinical AML blood samples and cultured AML cells. miR-204-5p was confirmed to be a target gene of LOC285758 by bioinformatics analysis and luciferase assay. LOC285758 overexpression promoted AML cell viability and invasion abilities, which were effectively inhibited by miR-204-5p overexpression; moreover, miR-204-5p overexpression also regulated the expression of E-cadherin, N-cadherin and Twist1. The data also showed that increased LOC285758 expression could effectively suppress the earlier effects of miR-204-5p on AML cells. Our findings suggest that targeting of miR-204-5p by LOC285758 promotes the cell viability and invasion of AML cells, and thus LOC285758 may have potential as a therapeutic target for AML treatment.
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