Epigenetic modulation and understanding of HDAC inhibitors in cancer therapy.

Acute myeloid leukemia (AML) is a common hematopoietic malignancy with a generally poor prognosis. Long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been identified as an oncogene in various malignancies including AML. However, the role and mechanisms of UCA1 in AML tumorigenesis were incompletely understood. Hence, this study aims to investigate whether UCA1 regulates AML progression by miR-296-3p/Myc axis. Cell proliferation and apoptosis were evaluated by MTT assay and flow cytometry, respectively. Luciferase reporter assay was performed to analyze the interaction between miR-296-3p and UCA1 or Myc. The results showed that UCA1 knockdown inhibited proliferation and induced apoptosis in AML cells (U937 and HL60). Mechanistically, UCA1 acted as a sponge of miR-296-3p by binding to miR-296-3p. Myc, a target of miR-296-3p, was positively regulated by UCA1. Functional assay showed that the anti-AML effect of UCA1 knockdown could be abrogated by miR-296-3p inhibition and Myc overexpression. Moreover, UCA1 knockdown inhibited AML cell tumorigenesis in vivo, which was associated with regulation of miR-296-3p and Myc expression. In conclusion, UCA1 modulates AML progression by regulating miR-296-3p/Myc axis.

Long non-coding RNA UCA1 modulates cell proliferation and apoptosis by regulating miR-296-3p/Myc axis in acute myeloid leukemia.

Long non-coding RNAs (lncRNAs) are biomarkers participating in multiple disease development including acute myeloid leukemia (AML). Here, we investigated molecular mechanism of X Inactive-Specific Transcript (XIST) in regulating cellular viability, apoptosis and drug resistance in AML. XIST, miR-29a and myelocytomatosis oncogene (MYC) expression in AML bone marrow cells collected from 62 patients was evaluated by RT-qPCR and Western blot analysis. Besides, the relationship among XIST, miR-29a and MYC was analyzed by dual luciferase reporter assay, RIP, and RNA pull down assays. AML KG-1 cells were treated with anti-tumor drug Adriamycin. The role of XIST/miR-29a/MYC in cellular viability, apoptosis and drug resistance in AML was accessed via gain- and loss-of-function approaches. At last, we evaluated role of XIST/miR-29a/MYC on tumorigenesis in vivo. XIST and MYC were up-regulated, and miR-29a was down-regulated in AML bone marrow cells. Silencing XIST inhibited cellular activity and drug resistance but promoted cellular apoptosis of KG-1 cells by down-regulating MYC. XIST inhibited miR-29a expression to up-regulate MYC. Moreover, silencing XIST inhibited tumorigenesis of AML cells in vivo. Overall, down-regulation of XIST decreased MYC expression through releasing the inhibition on miR-29a, thereby reducing drug resistance, inhibiting viability and promoting apoptosis of AML cells.

/pdf/silencing-long-non-coding-rna-xist-suppresses-drug-1iuccij51d.pdf

Silencing long non-coding RNA XIST suppresses drug resistance in acute myeloid leukemia through down-regulation of MYC by elevating microRNA-29a expression.

The aim of the present study was to examine the expression and clinical significance of long non-coding RNA (lncRNA)-CCDC26 in patients with acute myeloid leukemia (AML), and to investigate the potential functions of CCDC26. The Gene Expression Omnibus database and reverse transcription-quantitative polymerase chain reaction analysis were used to detect the expression levels of CCDC26 in patients with AML and healthy volunteers. Clinical data for 93 patients with AML were collected to analyze the clinical significance of CCDC26. Weighted gene co-expression network analysis (WGCNA), a protein-protein interaction (PPI) network, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to examine the functions of CCDC26. The expression levels of CCDC26 in the initially diagnosed and relapsed patients with AML were significantly upregulated compared with the control group. The upregulated expression level of CCDC26 in patients with AML was significantly associated with age, anemia, risk stratification and remission. Furthermore, patients with a high CCDC26 expression level had a poorer overall survival (P=0.0105). In addition, the area under the curve (AUC)1year and AUC2year of CCDC26 for overall survival were 0.722 and 0.686, respectively. WGCNA, PPI network and KEGG pathway analysis revealed that CCDC26 was involved in the regulation of a number of biological processes. lncRNA-CCDC26 may serve as a novel biomarker for monitoring the progression and predicting the clinical outcome of AML.

/pdf/lncrna-ccdc26-as-a-novel-biomarker-predicts-prognosis-in-4p7do11yil.pdf

lncRNA-CCDC26, as a novel biomarker, predicts prognosis in acute myeloid leukemia.

The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is a critical regulator for the development and progression of multiple tumors Yet, the role of SNHG1 in acute myeloid leukemia (AML) is unknown The present study demonstrated that SNHG1 expression was upregulated in AML SNHG1 silencing markedly repressed AML cell growth, whereas SNHG1 overexpression had the opposite effect MicroRNA-489-3p (miR-489-3p) was identified as a SNHG1-targeting miRNA SNHG1 knockdown increased miR-489-3p expression Low expression of miR-489-3p was correlated with high expression of SNHG1 in AML tissues miR-489-3p overexpression restricted AML cell growth, and SRY-related high-mobility-group box 12 (SOX12) was identified as a miR-489-3p-targeting gene SNHG1 inhibition or miR-489-3p overexpression inactivated Wnt/β-catenin signaling through downregulation of SOX12 SOX12 overexpression partially reversed the SNHG1 knockdown- or miR-489-3p overexpression-mediated effects Taken together, these data indicate that suppression of SNHG1 downregulates AML cell growth by inactivating SOX12/Wnt/β-catenin signaling via upregulating miR-489-3p

LncRNA SNHG1 contributes to the regulation of acute myeloid leukemia cell growth by modulating miR-489-3p/SOX12/Wnt/β-catenin signaling.

Long noncoding RNAs (lncRNAs) are a large family of noncoding RNAs that play a critical role in various normal bioprocesses as well as tumorigenesis. However, the expression patterns and biological functions of lncRNAs in acute leukemia have not been well studied. Here, we performed transcriptome-wide lncRNA expression profiling of acute myeloid leukemia (AML) patient samples, along with non-leukemia control hematopoietic samples. We found that lncRNAs were differentially expressed in AML samples relative to control samples. Notably, we identified that lncRNAs upregulated in AML (relative to the control samples) are associated with a lower degree of DNA methylation and a higher ratio of being bound by transcription factors such as SP1, STAT4, ATF-2 and ELK-1 compared with those downregulated in AML. Moreover, an enrichment of H3K4me3 and a depletion of H3K27me3 were observed in upregulated lncRNAs in AML. Expression patterns of three types of lncRNAs (antisense, enhancer and intergenic lncRNAs) have previously been characterized. Of the identified lncRNAs, we found that high expression level lncRNA LOC285758 is associated with the poor prognosis in AML patients. Furthermore, we found that LOC285758 regulates proliferation of AML cell lines by enhancing the expression of HDAC2, a key factor in carcinogenesis. Collectively, our study depicts a landscape of important lncRNAs in AML and provides novel potential therapeutic targets and prognostic markers for AML treatment.

Genome-wide characterization of lncRNAs in acute myeloid leukemia.

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Genome-wide characterization of lncRNAs in acute myeloid leukemia.