ArticleCancer research2011
MicroRNA-32 upregulation by 1,25-dihydroxyvitamin D3 in human myeloid leukemia cells leads to Bim targeting and inhibition of AraC-induced apoptosis.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- Tumor suppressor microRNAs, miR-100 and -125b, are regulated by 1,25-dihydroxyvitamin D in primary prostate cells and in patient tissue.Cancer prevention research (Philadelphia, Pa.) · 2013Trial
- MicroRNA Screening Reveals Upregulation of FoxO-Signaling in Relapsed Acute Myeloid Leukemia Patients.Genes · 2024Article
- Micro-RNAs in Response to Active Forms of Vitamin DInternational journal of molecular sciences · 2022Article
- Non-coding RNA-related antitumor mechanisms of marine-derived agents.Frontiers in pharmacology · 2022Review
- Mitochondrial metabolism as a target for acute myeloid leukemia treatment.Cancer & metabolism · 2021Review
- Regulatory noncoding RNAs: potential biomarkers and therapeutic targets in acute myeloid leukemia.American journal of blood research · 2021Article
- Eldecalcitol (ED-71)-induced exosomal miR-6887-5p suppresses squamous cell carcinoma cell growth by targeting heparin-binding protein 17/fibroblast growth factor-binding protein-1 (HBp17/FGFBP-1).In vitro cellular & developmental biology. Animal · 2020Article
- Virulence and Pathogenicity Properties ofPathogens (Basel, Switzerland) · 2019Review
- Assessment of temporal functional changes and miRNA profiling of human iPSC-derived cardiomyocytes.Scientific reports · 2019Article
- MiR-32-5p influences high glucose-induced cardiac fibroblast proliferation and phenotypic alteration by inhibiting DUSP1.BMC molecular biology · 2019Article
- Prenatal epigenetics diets play protective roles against environmental pollution.Clinical epigenetics · 2019Review
- Participation of vitamin D-upregulated protein 1 (TXNIP)-ASK1-JNK1 signalosome in the enhancement of AML cell death by a post-cytotoxic differentiation regimen.The Journal of steroid biochemistry and molecular biology · 2019Article
- New insights into vitamin D anticancer properties: focus on miRNA modulation.Molecular genetics and genomics : MGG · 2017Review
- microRNAs and Acute Myeloid Leukemia Chemoresistance: A Mechanistic Overview.Frontiers in oncology · 2017Review
- Therapeutic Resistance in Acute Myeloid Leukemia: The Role of Non-Coding RNAs.International journal of molecular sciences · 2016Review
- Current state of phenolic and terpenoidal dietary factors and natural products as non-coding RNA/microRNA modulators for improved cancer therapy and prevention.Non-coding RNA research · 2016Review
- Major apoptotic mechanisms and genes involved in apoptosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Extraskeletal actions of vitamin D.Annals of the New York Academy of Sciences · 2016Review
- The role of VDR and BIM in potentiation of cytarabine-induced cell death in human AML blasts.Oncotarget · 2016Article
- MicroRNA-551b is highly expressed in hematopoietic stem cells and a biomarker for relapse and poor prognosis in acute myeloid leukemia.Leukemia · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
1,25-Dihydroxyvitamin D(3) (1,25D) used to treat human acute myeloid leukemia (AML) cells induces features of normal monocytes, but the mechanisms underlying this response are not fully understood. We hypothesized that one or more microRNAs (miRNA) known to control mouse hematopoiesis and lineage commitment might contribute to the ability of 1,25D to control the malignant phenotype. Here we report that 1,25D markedly induces expression of miR-32 in human myeloid leukemia cells, in which it targets the 3'-untranslated region of the mRNA encoding the proapoptotic factor Bim to reduce its expression. RNAi-mediated suppression of the miRNA-processing enzymes Drosha and Dicer increased Bim levels, in support of the concept that Bim is under miRNA control in AML cells. Antisense-mediated suppression of miR-32 was sufficient to upregulate Bim expression in AML cells. Conversely, ectopic expression of miR-32 downregulated Bim expression and increased the differentiation response to 1,25D treatment in a manner that was associated with increased cell survival. The positive effects of miR-32 on cell survival were confirmed by evidence of increased cell death in AML cells preexposed to antisense miR-32 before treatment with arabinocytosine, a chemotherapeutic drug used to treat human AML. Together, our findings indicate that miR-32 blockade is sufficient to elevate Bim expression and sensitize AML cells to chemotherapy-induced apoptosis. Thus, agents which can inhibit miR-32 expression may offer clinical utility by enhancing therapeutic efficacy in human AML.
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