ArticleCancer medicine2021
A novel upregulated LncRNA-AC026150.8 promotes chemo-resistance and predicts poor prognosis in acute myeloid leukemia.
Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
- Non-coding RNAs in leukemia drug resistance: new perspectives on molecular mechanisms and signaling pathways.Annals of hematology · 2024Review
- Landscape of internal N7-methylguanosine of long non-coding RNA modifications in resistant acute myeloid leukemia.BMC genomics · 2023Article
- Long non-coding RNAs regulate treatment outcome in leukemia: What have we learnt recently?Cancer medicine · 2023Review
- A novel upregulated LncRNA-AC026150.8 promotes chemo-resistance and predicts poor prognosis in acute myeloid leukemia.Cancer medicine · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAML is a common hematological malignancy with poor prognosis, the pathogenesis is still unclear. lncRNA takes part in occurrence and development of AML. This research aims to explore new differentially expressed lncRNAs and their effects on AML.
methodsDatabase-based bioinformatics analysis was performed to screen differentially expressed lncRNA in AML, real-time PCR was used to analyze gene expression. Kaplan-Meier survival analysis was performed to determine prognostic effect of AC026150.8 in AML. The cell drug resistance experiment was performed to test effect of AC026150.8 on chemo-resistance of AML cells. Catrapid online software and RNA pull-down, mass spectrometry, western-blot were used to predict and verify the combination of AC026150.8 and RNA splicing factors.
resultsAC026150.8 was upregulated in AML patients and related to poor prognosis. High leukocyte counts, FAB classification, MLL-AF9 expression and NPM1 mutations were associated with high AC026150.8 expression. Upregulated of AC026150.8 increased the drug resistance of AML cells. AC026150.8 could be combined with splicing factor PCBP1.
conclusionsFor the first time, our study found that the upregulated AC026150.8 in AML is related to poor prognosis, overexpression of AC026150.8 could increase drug resistance of AML cells, and confirmed its scaffolding effect in combination with splicing factors. It is necessary to further study AC026150.8 and its downstream target genes to clarify the mechanism of AC026150.8 in AML.
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