ArticleCell death & disease2018
Aberrant mannosylation profile and FTX/miR-342/ALG3-axis contribute to development of drug resistance in acute myeloid leukemia.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 69 citations in OpenAlex.
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- Targeting miRNAs and Other Non-Coding RNAs as a Therapeutic Approach: An Update.Non-coding RNA · 2023Review
- Heat Shock Transcription Factor 2 Is Significantly Involved in Neurodegenerative Diseases, Inflammatory Bowel Disease, Cancer, Male Infertility, and Fetal Alcohol Spectrum Disorder: The Novel Mechanisms of Several Severe Diseases.International journal of molecular sciences · 2022Review
- The lncRNAs at X Chromosome Inactivation Center: Not Just a Matter of Sex Dosage Compensation.International journal of molecular sciences · 2022Review
- FTX Regulated miR-153-3p/FOXR2 to Promote Cisplatin Resistance in Ovarian Cancer.Computational and mathematical methods in medicine · 2022Article
- Mesenchymal stem cells in cancer progression and anticancer therapeutic resistance.Cancer cell international · 2021Review
- LncRNA UCA1 elevates the resistance of human leukemia cells to daunorubicin by the PI3K/AKT pathway via sponging miR-613.Bioscience reports · 2021Article
- ALG3 contributes to stemness and radioresistance through regulating glycosylation of TGF-β receptor II in breast cancer.Journal of experimental & clinical cancer research : CR · 2021Article
- A Nuclear Long Non-Coding RNA LINC00618 Accelerates Ferroptosis in a Manner Dependent upon Apoptosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
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- LncRNA FTX Involves in the Nogo-66-Induced Inhibition of Neurite Outgrowth Through Regulating PDK1/PKB/GSK-3β Pathway.Cellular and molecular neurobiology · 2020Article
- Sweet Control: MicroRNA Regulation of the Glycome.Biochemistry · 2020Review
- Knockdown of LncRNA CRNDE suppresses proliferation and P-glycoprotein-mediated multidrug resistance in acute myelocytic leukemia through the Wnt/β-catenin pathway.Bioscience reports · 2020Article
- LncRNA FTX activates FOXA2 expression to inhibit non-small-cell lung cancer proliferation and metastasis.Journal of cellular and molecular medicine · 2020Article
- Long noncoding RNA FTX ameliorates hydrogen peroxide-induced cardiomyocyte injury by regulating the miR-150/KLF13 axis.Open life sciences · 2020Article
- Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Long noncoding RNA ZFAS1 enhances adriamycin resistance in pediatric acute myeloid leukemia through the miR-195/Myb axis.RSC advances · 2019Article
Corrections and comments
- Retraction · 2020-02-12Concerns/Issues about Data · Duplication of Data · Objections by Author(s) ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Drug-resistance is a major problem in acute myeloid leukemia (AML) chemotherapy. Aberrant changes in specific N-glycans have been observed in leukemia multidrug resistance (MDR). MicroRNAs (miRNAs) and long non coding RNAs (lncRNAs) act as key players in the development of AML resistance to chemotherapy. In the present study, the N-glycan profiles of membrane proteins were analyzed from adriamycin (ADR)-resistant U937/ADR cells and sensitive line U937 cells using mass spectrometry (MS). The composition profiling of high-mannose N-glycans differed in U937/ADR and U937 cell lines. Lectin microarray showed that the strong binding of membrane proteins was observed for MAN-M and ConA lectins, which were specific for mannose. These binding were also validated by flow cytometry. Importantly, the alteration of high-mannose N-glycan was further confirmed by detecting the enzyme level of ALG family. The altered level of ALG3 was found corresponding to the drug-resistant phenotype of AML cell lines both in vitro and in vivo. Mechanistically, miR-342 was found to be dysregulated and inversely correlated to ALG3 expression, targeting its 3'-UTR. LncRNA FTX was a direct target of miR-342 and positively modulated ALG3 expression by competitively binding miR-342 in AML cell lines. Functionally, we found that FTX directly interacted with miR-342 to regulate ALG3 expression and function, including ADR-resistant cell growth and apoptosis. The observation suggested that high-mannose N-glycans and mannosyltransferase ALG3 affected drug-resistance in AML cells. FTX/miR-342/ALG3 axis could potentially be used for the targets to overcome therapeutic resistance in AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.