MicroRNA-363-3p promote the development of acute myeloid leukemia with RUNX1 mutation by targeting SPRYD4 and FNDC3B

Chen, Yimin; Chen, Shuyi; Lu, Jielun; Yuan, Danyun; He, Lang; Qin, Pengfei; H, Tan; Xu, Lihua

doi:10.1097/md.0000000000025807

Cited by 12 publications

(7 citation statements)

References 49 publications

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“…To the best of our knowledge, miR-363-3p has been revealed to play an important role in the pathogenic processes of malignant tumors, including proliferation, apoptosis, and epithelial-mesenchymal transition in colorectal cancer ( 38 ), lung cancer ( 39 ), retinoblastoma ( 40 ), oral squamous cell carcinoma ( 41 ), and acute myeloid leukemia ( 42 ). Recent studies have reported that miR-363-3p as a stroke neuroprotectant could improve ischemic stroke outcomes in female rats ( 15 , 16 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP

Wang

Jin

Xia³

et al. 2022

Mol Med Rep

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The purpose of the present study was to explore the functional role of microrna (mir)-363-3p and related regulatory mechanisms in cerebral ischemia/reperfusion (i/r) injury. The neuronal cell line SH-SY5Y was exposed to 4 h of oxygen and glucose deprivation (oGd), followed by 6, 12, 24 and 48 h of re-oxygenation to mimic i/r injury in vitro. Cell viability, apoptosis and inflammation were assessed by ccK-8, lactate dehydrogenase (ldH), flow cytometry and eliSa assays. The association between mir-363-3p and programmed cell death 6-interacting protein (Pdcd6iP) was further confirmed using luciferase reporter assay. our data revealed that the expression level of miR-363-3p was significantly downregulated after oGd/r induction. overexpression of mir-363-3p markedly suppressed OGD/R-induced cell injury, as reflected by attenuated cell viability, reduced apoptosis, ldH activity and pro-inflammatory cytokine levels. Mechanistically, Pdcd6iP was confirmed as the target of mir-363-3p. Furthermore, Pdcd6iP knockdown imitated, while overexpression reversed the effects of mir-363-3p overexpression on oGd/r-induced cell injury. collectively, mir-363-3p could attenuate oGd/r-induced cell injury by alleviating apoptosis and inflammation, which may be mediated, at least in part, via inhibition of Pdcd6iP.

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Section: Discussionmentioning

confidence: 99%

miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP

Wang

Jin

Xia³

et al. 2022

Mol Med Rep

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“…Although miR-874-3p was found to be overexpressed in MDS and AML patients, its downregulation by DANCR through sponging may contribute to cytarabine resistance in AML by activating autophagy [41,42]. Finally, miR-363-3p promotes the development of RUNX1-mutated AML and affects expression of tumor suppressor genes in T-ALL, modulating survival [43,44].…”

Section: Discussionmentioning

confidence: 99%

Deciphering the Non-Coding RNA Landscape of Pediatric Acute Myeloid Leukemia

Vanhooren

Camp

Depreter

et al. 2022

Cancers

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Pediatric acute myeloid leukemia (pedAML) is a heterogeneous blood cancer that affects children. Although survival rates have significantly improved over the past few decades, 20–30% of children will succumb due to treatment-related toxicity or relapse. The molecular characterization of the leukemic stem cell, shown to be responsible for relapse, is needed to improve treatment options and survival. Recently, it has become clear that non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), play a role in the development of human diseases, including pediatric cancer. Nevertheless, non-coding RNA expression data in pedAML are scarce. Here, we explored lncRNA (n = 30168) and miRNA (n = 627) expression in pedAML subpopulations (leukemic stem cells (LSCs) and leukemic blasts (L-blasts)) and their normal counterparts (hematopoietic stem cells and control myeloblasts). The potential regulatory activity of differentially expressed lncRNAs in LSCs (unique or shared with the L-blast comparison) on miRNAs was assessed. Moreover, pre-ranked gene set enrichment analyses of (anti-) correlated protein-coding genes were performed to predict the functional relevance of the differentially upregulated lncRNAs in LSCs (unique or shared with the L-blast comparison). In conclusion, this study provides a catalog of non-coding RNAs with a potential role in the pathogenesis of pedAML, paving the way for further translational research studies.

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“… 52 It was found that Mgst1 deletion in mice resulted in embryonic lethal and impaired haematopoietic function, emphasizing that Mgst1 is essential for embryonic development and haematopoietic function in vertebrates. 53 SPRYD4 has not been widely explored, but it has been recently found to have anti-cancer effects, such as acute myeloid leukemia 54 and hepatocellular carcinoma. 55 In our GO annotation, glutathione peroxidase activity was also found to involve in vertigo by Banner PWAS.…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of proteome-wide and transcriptome-wide association studies identified novel genes and chemicals for vertigo

Cheng

Meng

Yang

et al. 2022

Brain Communications

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Vertigo is a leading symptom of various peripheral and central vestibular disorders. Although genome-wide association studies (GWAS) have identified multiple risk variants for vertigo, how these risk variants contribute to the risk of vertigo remains unknown. Discovery proteome-wide association study (PWAS) was first performed by integrating the protein quantitative trait loci from dorsolateral prefrontal cortex (DLPFC) in Banner Sun Health Research Institute dataset (N = 152) and GWAS summary of vertigo (N = 942,613), followed by replication PWAS using the protein quantitative trait loci from the DLPFC in Religious Orders Study or the Rush Memory and Aging Project dataset (N = 376). Transcriptome-wide association studies (TWASs) were then performed by integrating the same GWAS datasets of vertigo (N = 942,613) with mRNA expression reference from human fetal brain, and DLPFC. Chemical-related gene set enrichment analysis (GSEA) and Gene ontology/Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were finally conducted to further reveal the pathogenesis of vertigo. Permutation-based empirical P values were calculated in PWAS, TWAS and GSEA. By integrating the GWAS of vertigo and two independent brain proteomes from human DLPFC, 3 genes were identified to genetically regulate protein abundance levels in vertigo, and were not previously implicated by GWAS, including MTERFD2 (PBanner = 0.045, PROSMAP = 0.031), MGST1 (PBanner = 0.014, PROSMAP = 0.018), and RAB3B (PBanner = 0.045, PROSMAP = 0.035). Compared with TWAS results, we identified overlapping genes RAB3B (PTWAS = 0.017) and MTERFD2 (PTWAS = 0.003) that showed significant associations with vertigo at both proteome-wide and transcriptome-wide levels. Chemical-related GSEA identified multiple chemicals that might be associated with vertigo, such as nickel (P = 0.007), glycidamide (P = 0.005), and proanthocyanidins (P = 0.015). Our study provides novel clues for understanding the biological mechanism of vertigo, and highlights several possible risks and therapeutic chemicals for vertigo.

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MicroRNA-363-3p promote the development of acute myeloid leukemia with RUNX1 mutation by targeting SPRYD4 and FNDC3B

Cited by 12 publications

References 49 publications

miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP

miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injury in vitro by targeting PDCD6IP

Deciphering the Non-Coding RNA Landscape of Pediatric Acute Myeloid Leukemia

Integrated analysis of proteome-wide and transcriptome-wide association studies identified novel genes and chemicals for vertigo

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