ABSTRACT
High-magnetization materials play crucial roles in various applications. However, the past few decades have witnessed a stagnation in the discovery of new materials with high magnetization. In this work, Ni/NiO nanocomposites are fabricated by depositing Ni and NiO thin layers alternately, followed by annealing at specific temperatures. Both the as-deposited samples and those annealed at 373 K exhibit low magnetization. However, the samples annealed at 473 K exhibit a significantly enhanced saturation magnetization exceeding 607 emu cm-3 at room temperature, surpassing that of pure Ni (480 emu cm-3 ). Material characterizations indicate that the composite comprises NiO nanoclusters of size 1-2 nm embedded in the Ni matrix. This nanoclustered NiO is primarily responsible for the high magnetization, as confirmed by density functional theory calculations. The calculations also indicate that the NiO clusters are ferromagnetically coupled with Ni, resulting in enhanced magnetization. This work demonstrates a new route toward developing artificial high-magnetization materials using the high magnetic moments of nanoclustered antiferromagnetic materials.
ABSTRACT
Hematologic malignancies are the most common hematopoietic diseases and a major public health concern. However, the mechanisms underlying myeloid tumors remain unknown owing to the intricate interplay between mutations and diverse clonal evolution patterns, as evidenced by the analysis of bulk cell-derived omics data. Several single-cell omics techniques have been used to characterize the hierarchies and altered immune microenvironments of hematologic malignancies. The comprehensive single-cell atlas of hematologic malignancies provides novel opportunities for personalized combinatorial targeted treatments, avoiding unwanted chemo-toxicity. In the present study, we performed transcriptome sequencing by combining single-cell RNA sequencing (scRNA-seq) with a targeted oncogenic gene panel for acute myeloid leukemia, overcoming the limitations of scRNA-seq in detecting oncogenic mutations. The distribution of oncogenic IDH1, IDH2, and KRAS mutations in each cell type was identified in the bone marrow (BM) samples of each patient. Our findings suggest that ferroptosis and metabolic reprogramming are involved in the tumorigenesis and chemotherapy resistance of oncogenic mutation-carrying cells. Biological progression via IDH1, IDH2, and KRAS mutations arrests hematopoietic maturation. Our study findings provide a rationale for using primary BM cells for personalized treatment in clinical settings.
Subject(s)
Ferroptosis , Hematologic Neoplasms , Humans , Proto-Oncogene Proteins p21(ras)/genetics , Hematologic Neoplasms/drug therapy , Hematologic Neoplasms/genetics , Mutation , Sequence Analysis, RNA , Tumor MicroenvironmentABSTRACT
BACKGROUND: Approximately 8-9% of the world's population is affected by autoimmune diseases, and yet the mechanism of autoimmunity trigger is largely understudied. Two unique cell death modalities, ferroptosis and pyroptosis, provide a new perspective on the mechanisms leading to autoimmune diseases, and development of new treatment strategies. METHODS: Using scRNA-seq datasets, the aberrant trend of ferroptosis and pyroptosis-related genes were analyzed in several representative autoimmune diseases (psoriasis, atopic dermatitis, vitiligo, multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and experimental autoimmune orchitis). Cell line models were also assessed using bulk RNA-seq and qPCR. RESULTS: A substantial difference was observed between normal and autoimmune disease samples involving ferroptosis and pyroptosis. In the present study, ferroptosis and pyroptosis showed an imbalance in different keratinocyte lineages of psoriatic skinin addition to a unique pyroptosis-sensitive keratinocyte subset in atopic dermatitis (AD) skin. The results also revealed that pyroptosis and ferroptosis are involved in epidermal melanocyte destruction in vitiligo. Aberrant ferroptosis has been detected in multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and autoimmune orchitis. Cell line models adopted in the study also identified pro-inflammatory factors that can drive changes in ferroptosis and pyroptosis. CONCLUSION: These results provide a unique perspective on the involvement of ferroptosis and pyroptosis in the pathological process of autoimmune diseases at the scRNA-seq level. IFN-γ is a critical inducer of pyroptosis sensitivity, and has been identified in two cell line models.
Subject(s)
Autoimmune Diseases , Crohn Disease , Dermatitis, Atopic , Ferroptosis , Lung Diseases, Interstitial , Multiple Sclerosis , Orchitis , Scleroderma, Systemic , Vitiligo , Autoimmune Diseases/genetics , Crohn Disease/genetics , Humans , Male , Pyroptosis/genetics , Sclerosis , Transcriptome/genetics , Vitiligo/geneticsABSTRACT
Intestinal microbiota is an important prognostic factor for allogeneic hematopoietic stem cell transplantation (allo-HSCT), but its role in predicting survival has not been determined. Here, stool samples at day 15 ± 1 posttransplant were obtained from 209 patients at two centers. Microbiota was examined using 16S rRNA sequencing. The microbiota diversity and abundance of specific bacteria (including Lachnospiraceae, Ruminococcaceae, Erysipelotrichaceae, and Enterobacteriaceae) were assigned a value of 0 or 1 depending on whether they were positive or negative associated with survival, respectively. An accumulated intestinal microbiota (AIM) score was generated, and patients were divided into low- and high-score groups. A low score was associated with a better 3-year cumulative overall survival (OS) as well as lower mortality than a high score (88.5 vs. 43.9% and 7.1 vs. 35.8%, respectively; both P < 0.001). In multivariate analysis, a high score was found to be an independent risk factor for OS and transplant-related mortality (hazard ratio = 5.68 and 3.92, respectively; P < 0.001 and 0.003, respectively). Furthermore, the AIM score could serve as a predictor for survival (area under receiver operating characteristic curve = 0.836, P < 0.001). Therefore, the intestinal microbiota score at neutrophil recovery could predict survival following allo-HSCT.
Subject(s)
Gastrointestinal Microbiome , Graft vs Host Disease , Hematopoietic Stem Cell Transplantation , Microbiota , Firmicutes/genetics , Graft vs Host Disease/etiology , Graft vs Host Disease/microbiology , Humans , RNA, Ribosomal, 16S/geneticsABSTRACT
Anthocyanins, vital metabolites in plants, are formed by anthocyanidins combined with various monosaccharides, including glucose, rhamnose, and arabinose. Rhamnose contributes greatly to the glycosylation of anthocyanidins. There are two kinds of rhamnose synthase (RS): rhamnose biosynthesis (RHM), and nucleotide-RS/epimerase-reductase (UER1). Nevertheless, no RS isoform was reported to be involved in anthocyanin synthesis. Here, three homologous PhRHM genes, namely PhRHM1, PhRHM2, and PhRHM3, and one PhUER1 gene from petunia were cloned and characterized. Green fluorescent protein fusion protein assays revealed that PhRHMs and PhUER1 are localized in the cytoplasm. We obtained PhRHM1 or/and PhRHM2 or PhUER1 silenced petunia plants and did not attempt to obtain PhRHM3 silenced plants since PhRHM3 mRNA was not detected in petunia organs examined. PhRHM1 and PhRHM2 (PhRHM1-2) silencing induced abnormal plant growth and decreased the contents of l-rhamnose, photosynthetic pigments and total anthocyanins, while PhUER1 silencing did not cause any visible phenotypic changes. Flavonoid metabolome analysis further revealed that PhRHM1-2 silencing reduced the contents of anthocyanins with rhamnose residue. These results revealed that PhRHMs contribute to the biosynthesis of rhamnose and that PhRHMs participate in the anthocyanin rhamnosylation in petunia, while PhUER1 does not.
Subject(s)
Petunia , Petunia/genetics , Anthocyanins/metabolism , Rhamnose/metabolism , Arabinose/metabolism , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Gene Expression Regulation, Plant , Flowers/genetics , Flowers/metabolism , Plant Leaves/metabolism , Flavonoids/metabolism , Oxidoreductases/metabolism , Glucose/metabolism , Nucleotides/metabolism , Racemases and Epimerases/genetics , Racemases and Epimerases/metabolismABSTRACT
BACKGROUND: Senescence represents the last stage of flower development. Phosphorylation is the key posttranslational modification that regulates protein functions, and kinases may be more required than phosphatases during plant growth and development. However, little is known about global phosphorylation changes during flower senescence. RESULTS: In this work, we quantitatively investigated the petunia phosphoproteome following ethylene or air treatment. In total, 2170 phosphosites in 1184 protein groups were identified, among which 2059 sites in 1124 proteins were quantified. To our surprise, treatment with ethylene resulted in 697 downregulated and only 117 upregulated phosphosites using a 1.5-fold threshold (FDR < 0.05), which showed that ethylene negatively regulates global phosphorylation levels and that phosphorylation of many proteins was not necessary during flower senescence. Phosphoproteome analysis showed that ethylene regulates ethylene and ABA signalling transduction pathways via phosphorylation levels. One of the major targets of ethylene-induced dephosphorylation is the plant mRNA splicing machinery, and ethylene treatment increases the number of alternative splicing events of precursor RNAs in petunia corollas. CONCLUSIONS: Protein dephosphorylation could play an important role in ethylene-induced senescence, and ethylene treatment increased the number of AS precursor RNAs in petunia corollas.
Subject(s)
Flowers/metabolism , Petunia/metabolism , Plant Proteins/metabolism , Plants/metabolism , Proteome/metabolism , Aging/physiology , Ethylenes/metabolism , Flowers/genetics , Gene Expression Regulation, Plant , Petunia/genetics , Plant Proteins/genetics , Plants/genetics , Proteome/geneticsABSTRACT
In recent years, atomically thin superconductors, including atomically thin elemental superconductors, single layer FeSe films, and few-layer cuprate superconductors, have been studied extensively. This hot research field is mainly driven by the discovery of significant superconductivity enhancement and high-temperature interface superconductivity in single-layer FeSe films epitaxially grown on SrTiO3 substrates in 2012. This study has attracted tremendous research interest and generated more studies focusing on further enhancing superconductivity and finding the origin of the superconductivity. A few years later, research on atomically thin superconductors has extended to cuprate superconductors, unveiling many intriguing properties that have neither been proposed or observed previously. These new discoveries challenge the current theory regarding the superconducting mechanism of unconventional superconductors and indicate new directions on how to achieve high-transition-temperature superconductors. Herein, this exciting recent progress is briefly discussed, with a focus on the recent progress in identifying new atomically thin superconductors.
ABSTRACT
The spin-gapless semiconductors (SGSs) are a new class of zero-gap materials which have fully spin polarized electrons and holes. They bridge the zero-gap materials and the half-metals. The band structures of the SGSs can have two types of energy dispersion: Dirac linear dispersion and parabolic dispersion. The Dirac-type SGSs exhibit fully spin polarized Dirac cones, and offer a platform for massless and fully spin polarized spintronics as well as dissipationless edge states via the quantum anomalous Hall effect. With fascinating spin and charge states, they hold great potential for spintronics. There have been tremendous efforts worldwide to find suitable candidates for SGSs. In particular, there is an increasing interest in searching for Dirac type SGSs. In the past decade, a large number of Dirac or parabolic type SGSs have been predicted by density functional theory, and some parabolic SGSs have been experimentally demonstrated. The SGSs hold great potential for spintronics, electronics, and optoelectronics with high speed and low-energy consumption. Here, both the Dirac and the parabolic types of SGSs in different material systems are reviewed and the concepts of the SGS, novel spin and charge states, and the potential applications of SGSs in next-generation spintronic devices are outlined.
ABSTRACT
Cytosolic acetyl-CoA is an intermediate of the synthesis of most secondary metabolites and the source of acetyl for protein acetylation. The formation of cytosolic acetyl-CoA from citrate is catalysed by ATP-citrate lyase (ACL). However, the function of ACL in global metabolite synthesis and global protein acetylation is not well known. Here, four genes, PaACLA1, PaACLA2, PaACLB1, and PaACLB2, which encode the ACLA and ACLB subunits of ACL in Petunia axillaris, were identified as the same sequences in Petunia hybrida 'Ultra'. Silencing of PaACLA1-A2 and PaACLB1-B2 led to abnormal leaf and flower development, reduced total anthocyanin content, and accelerated flower senescence in petunia 'Ultra'. Metabolome and acetylome analysis revealed that PaACLB1-B2 silencing increased the content of many downstream metabolites of acetyl-CoA metabolism and the levels of acetylation of many proteins in petunia corollas. Mechanistically, the metabolic stress induced by reduction of acetyl-CoA in PaACL-silenced petunia corollas caused global and specific changes in the transcriptome, the proteome, and the acetylome, with the effect of maintaining metabolic homeostasis. In addition, the global proteome and acetylome were negatively correlated under acetyl-CoA deficiency. Together, our results suggest that ACL acts as an important metabolic regulator that maintains metabolic homeostasis by promoting changes in the transcriptome, proteome. and acetylome.
Subject(s)
Petunia , Proteome , ATP Citrate (pro-S)-Lyase , Acetyl Coenzyme A , Flowers/genetics , Homeostasis , Petunia/geneticsABSTRACT
OBJECTIVE: To investigate the expression of cystic fibrosis transmembrane conductance regulator (CFTR) protein in patients with acute leukemia and its relationship to clinical features and prognosis of acute leukemia. METHODS: A total of115 patients with acute leukemia were enrolled in the experimental group and 20 healthy individuals were used as control. Peripheral blood or bone marrow samples were collected, and mononuclear cells were isolated. The expression of CFTR protein was detected by Western blot. The relationships of CFTR protein expression to clinical features and prognosis was analyzed. RESULTS: The expression of CFTR protein was not detected in peripheral blood mononuclear cells of normal control, while it was positive in more than half of acute leukemias including acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), but negative in the patients with acute promyelocytic leukemia (M3). In the patients with AML, there was no difference in peripheral white blood cells (WBC), peripheral blast cells, platelet and hemoglobin (HGB) between CFTR-positive and CFTR-negative patients. There was no relationship between the expression of CFTR protein and gene mutations such as NPM1, CEBPA, FLT3-ITD, and C-Kit. Complete remission (CR) rate after two course in CFTR-negative patients was slightly higher than that in positive patients. The survival time of CFTR-negative patients was little longer than that of positive patients, but the difference was not statistically significant. CONCLUSIONS: The expression of CFTR protein seems not associated with clinical features, treatment response and prognosis in the patients with acute leukemia.
Subject(s)
Cystic Fibrosis Transmembrane Conductance Regulator/genetics , Leukemia, Myeloid, Acute/genetics , Humans , Leukemia, Myeloid, Acute/diagnosis , Leukocytes, Mononuclear , Mutation , Nucleophosmin , PrognosisABSTRACT
We have carried out a detailed investigation of the magnetism, valence state, and magnetotransport in VSe2 bulk single crystals, as well as in laminates obtained by mechanical exfoliation. In sharp contrast to the ferromagnetic behavior reported previously, here, no ferromagnetism could be detected for VSe2 single crystal and laminate from room temperature down to 2 K. Neither did we find the Curie paramagnetism expected due to the 3d 1 odd-electronic configuration of covalent V4+ ions. Rather, intrinsic VSe2 is a non-magnetic alloy without local moment. Only a weak paramagnetic contribution introduced by defects is noticeable below 50 K. A weak localization effect due to defects was also observed in VSe2 single crystals for the first time.
ABSTRACT
HLA-DPA1*02:117 differs from HLA-DPA1*02:02:02:01 by one nucleotide in exon 2.
Subject(s)
HLA-DP alpha-Chains , Nucleotides , Humans , Alleles , HLA-DP alpha-Chains/genetics , China , Sequence Analysis, DNAABSTRACT
Aplastic anemia (AA) is a bone marrow (BM) failure syndrome mediated by hyperactivated T-cells with heterogeneous pathogenic factors. The onset of BM failure cannot be accurately determined in humans; therefore, exact pathogenesis remains unclear. In this study, a cellular atlas and microenvironment interactions is established using unbiased single-cell RNA-seq, along with multi-omics analyses (mass cytometry, cytokine profiling, and oxidized fatty acid metabolomics). A new KIR+ CD8+ regulatory T cells (Treg) subset is identified in patients with AA that engages in immune homeostasis. Conventional CD4+ T-cells differentiate into highly differentiated T helper cells with type 2 cytokines (IL-4, IL-6, and IL-13), GM-SCF, and IL-1ß. Immunosuppressive homeostasis is impaired by enhanced apoptosis of activated Treg cells. Pathological Vδ1 cells dominated the main fraction of γδ T-cells. The B/plasma, erythroid, and myeloid lineages also exhibit substantial pathological features. Interactions between TNFSF12-TNFRSF12A, TNF-TNFRSF1A, and granzyme-gasdermin are associated with the cell death of hematopoietic stem/progenitor (HSPCs), Treg, and early erythroid cells. Ferroptosis, a major driver of HSPCs destruction, is identified in patients with AA. Furthermore, a case of twins with AA is reported to enhance the persuasiveness of the analysis. These results collectively constitute the cellular atlas and microenvironment interactions in patients with AA and provide novel insights into the development of new therapeutic opportunities.
Subject(s)
Anemia, Aplastic , Humans , Anemia, Aplastic/pathology , Bone Marrow Cells/pathology , Hematopoietic Stem Cells/metabolism , Hematopoiesis/physiology , Cytokines/metabolismABSTRACT
Risk stratification for normal karyotype acute myeloid leukemia (NK-AML) remains unsatisfactory, which is reflected by the high incidence of leukemia relapse. This study aimed to evaluate the role of gene mutations and clinical characterization in predicting the relapse of patients with NK-AML. A prognostic system for NK-AML was constructed. A panel of gene mutations was explored using next-generation sequencing. A nomogram algorithm was used to build a genomic mutation signature (GMS) nomogram (GMSN) model that combines GMS, measurable residual disease, and clinical factors to predict relapse in 347 patients with NK-AML from four centers. Patients in the GMS-high group had a higher 5-year incidence of relapse than those in the GMS-low group (p < 0.001). The 5-year incidence of relapse was also higher in patients in the GMSN-high group than in those in the GMSN-intermediate and -low groups (p < 0.001). The 5-year disease-free survival and overall survival rates were lower in patients in the GMSN-high group than in those in the GMSN-intermediate and -low groups (p < 0.001) as confirmed by training and validation cohorts. This study illustrates the potential of GMSN as a predictor of NK-AML relapse.
Subject(s)
Leukemia, Myeloid, Acute , Nucleophosmin , Humans , Mutation , Prognosis , Chronic Disease , Leukemia, Myeloid, Acute/genetics , Recurrence , KaryotypeABSTRACT
N6-methyladenosine (m6A) is the most abundant internal modification in mammalian mRNA and recent studies have highlighted the importance of m6A levels in tumor development. In this study, we investigated the expression of methyltransferase-like 3 (METTL3) and 14 (METTL14), components of the RNA m6A methyltransferase complex, in samples from 89 patients with acute myeloid leukemia (AML), and followed the survival of 75 of these patients. Our results show that METTL3 and METTL14 are highly expressed in most of the patients with AML (except those with APL), and high levels of METTL3 and/or METTL14 correlated to shorter survival in the patients. In leukemia cell lines K562 and kasumi-1, both METTL3 and METTL14 promote cell proliferation and cell cycle, and the knockdown of METTL3 and METTL14 inhibits proliferation, and induces apoptosis and differentiation. Notably, the knockdown of METTL3 and METTL14 in K562 cell line leads to several changes in the expression of p53 signal pathway, including the upregulation of p53, cyclin dependent kinase inhibitor 1A (CDKN1A/p21), and downregulation of mdm2. Importantly, the m6A level of mdm2 mRNA was significant lower after knock-down of METTL3 and METTL14 examined by m6A-RIP and mdm2 qPCR assay, and the half-life of mdm2 under actinomycin-D treatment became shorter. Taken together, our study demonstrates that the lower m6A levels of mdm2 mRNA mediated by the knockdown of METTL3 and METTL14 could lead to the low stability of mdm2 mRNA transcripts and low expression of MDM2, in the end, activate p53 signal pathway. Both METTL3 and METTL14 play an oncogenic role in AML by targeting mdm2/p53 signal pathway.
ABSTRACT
It is well known that the existence of interstitial Fe is a great obstacle to enhancing the superconducting properties of the Fe(Se, Te) system. In this work, a silver and oxygen codoping effect toward enhancement of the superconductivity and flux pinning in Fe(Se, Te) bulks is reported. The oxygen ions from SeO2 can induce the precipitation of interstitial Fe as Fe2O3, thus simultaneously optimizing the superconducting properties of Fe(Se, Te) and forming extra flux pinning centers, while the existence of Ag can enhance the intergrain connections of the polycrystalline material by improving the electron transport at grain boundaries. Compared with the undoped sample, the critical current density, the upper critical field, and the thermally activated flux flow activation energy are greatly enhanced by 4.7, 1.7, and 1.5 times, respectively. The novel synthesis technique and optimized properties of this work can pave the way for the development of high-performance Fe(Se, Te) superconducting wires or tapes.
ABSTRACT
OBJECTIVES: This study retrospectively investigated in which cycle measurable residual disease (MRD) is associated with prognosis in patients in first complete remission (CR1) of intermediate-risk acute myeloid leukemia (AML). METHODS: The study enrolled 235 younger patients with intermediate-risk AML. MRD was evaluated by multiparameter flow cytometry after the 1st, 2nd, and 3rd chemotherapy cycles (MRD1-3, respectively). RESULTS: No significant association was detected after the 1st and 2nd cycles. However, the 5-year incidence of relapse was higher in the MRD3-positive group (n = 99) than in the negative group (n = 136) (48.7% vs. 13.7%, P = 0.005), while 5-year disease-free survival (DFS) and overall survival (OS) were lower in the MRD3-positive group than in the negative group (43.2% vs. 81.0% and 45.4% vs. 84.1%; P = 0.003 and 0.005, respectively). Allogeneic hematopoietic stem cell transplantation led to a lower 5-year relapse, and higher DFS and OS rates than chemotherapy in the MRD3-positive group (22.3% vs. 71.5%, 65.9% vs. 23.0%, and 67.1% vs. 23.9%; P < 0.001, 0.002, and 0.022, respectively), but did not affect the MRD-negative group. CONCLUSIONS: MRD3 could serve as an indicator for post-remission treatment choice and help improve outcomes for intermediate-risk AML in CR1.
Subject(s)
Hematopoietic Stem Cell Transplantation , Leukemia, Myeloid, Acute , Humans , Transplantation, Homologous , Retrospective Studies , Leukemia, Myeloid, Acute/therapy , Neoplasm, Residual , Remission Induction , Prognosis , Recurrence , Receptors, Complement 3bABSTRACT
Anthocyanins are important flavonoid pigments in plants. Malonyl CoA is an important intermediate in anthocyanin synthesis, and citrate, formed by citrate synthase (CS) catalysing oxaloacetate, is the precursor for the formation of malonyl-CoA. CS is composed of two isoforms, mitochondrial citrate synthase (mCS), a key enzyme of the tricarboxylic acid (TCA) cycle, and citrate synthase (CSY) localizated in microbodies in plants. However, no CS isoform involvement in anthocyanin synthesis has been reported. In this study, we identified the entire CS family in petunia (Petunia hybrida): PhmCS, PhCSY1 and PhCSY2. We obtained petunia plants silenced for the three genes. PhmCS silencing resulted in abnormal development of leaves and flowers. The contents of citrate and anthocyanins were significantly reduced in flowers in PhmCS-silenced plants. However, silencing of PhCSY1 and/or PhCSY2 did not cause a visible phenotype change in petunia. These results showed that PhmCS is involved in anthocyanin synthesis and the development of leaves and flowers, and that the citrate involved in anthocyanin synthesis mainly derived from mitochondria rather than microbodies in petunia.
Subject(s)
Anthocyanins/biosynthesis , Anthocyanins/genetics , Citrate (si)-Synthase/genetics , Citrate (si)-Synthase/metabolism , Flowers/enzymology , Flowers/genetics , Petunia/enzymology , Petunia/genetics , Gene Expression Regulation, Plant , Genes, MitochondrialABSTRACT
PURPOSE: Acute myeloid leukemia (AML) is a heterogenous disease and the survival of AML patients is largely attributed to the improvement of supportive treatment. Wilms' tumor 1-associated protein (WTAP) is a nuclear protein functions in many physiological and pathological processes. Although its expression and function in many malignant diseases have been reported, its prognostic and epigenetic roles in AML are largely unknown. METHODS: Peripheral blood or bone marrow samples were collected from AML patients. The WTAP expression was detected by western blot. WTAP expression level and patients clinical features were analyzed using statistical methods. WTAP knockdown AML cells were constructed. The experiments on proliferation, tumorigenic ability, cell cycle, and apoptosis were performed. Transcriptome sequencing was performed and analyzed. M6A methylation level was measured and m6A-RIP was performed to quantify m6A methylation level of MYC mRNA. RNA stability assay was performed to measure the half-life of mRNA. RESULTS: WTAP was overexpressed in AML patients and was an independent poor-risk factor in AML (p = 0.0140). Moreover, we found that WTAP regulated proliferation, tumorigenesis, cell cycle, and differentiation of AML cells. Furthermore, WTAP made AML cells resistant to daunorubicin. In further investigations, m6A methylation level was downregulated when knocking down WTAP, and c-Myc was upregulated due to the decreased m6A methylation of MYC mRNA. CONCLUSION: High WTAP expression predicts poor prognosis in AML and WTAP plays an epigenetic role in AML.