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LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia (Affymetrix)

ABSTRACT: Long non-coding RNAs (lncRNAs) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by RT-qPCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65646 | GEO | 2015/02/05

SECONDARY ACCESSION(S): PRJNA274651

REPOSITORIES: GEO

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LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia (Affymetrix)

Project description:Long non-coding RNAs (lncRNAs) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by RT-qPCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development. To define gene expression changes attributable to expression of lncRNAs, we transduced RS4;11 cells with a siRNA against BALR-2 or control vector. These cells were left untreated or treated with prednisolone.

2015-02-05 | E-GEOD-65646 | biostudies-arrayexpress

LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia (Agilent)

2015-02-05 | GSE65645 | GEO

LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia (Agilent)

Project description:Long non-coding RNAs (lncRNAs) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by RT-qPCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development. B-lymphoblastic leukemia is characterized by several translocations. In this study, we hybridized patient bone marrow samples from a total of 44 patients including 14 patients with B-ALL carrying a TEL-AML1 translocation, 15 patients with E2A-PBX1 translocation, and 15 patients carrying MLL translocations. The hybridizations were carried out in two sets, a discovery set and a validation set. In addition, we utilized samples from a human cell line (NALM6) and control CD10+CD19+ cells from human bone marrow.

2015-02-05 | E-GEOD-65645 | biostudies-arrayexpress

Gene expression data from children diagnosed with ALL in vitro sensitive or resistant to prednisolone

2009-12-16 | GSE19143 | GEO

Computational prediction and experimental validation identify functionally conserved lncRNAs from zebrafish to human

Project description:Functional studies of long noncoding RNAs (lncRNAs) have long been hindered by a lack of methods to assess their evolution. Here, we present lncHOME (lncRNA Homology Explorer), a computational pipeline that identifies a unique coPARSE-lncRNA class with conserved genomic locations and patterns of RNA binding protein (RBP) binding sites. Remarkably, several hundred human coPARSE-lncRNAs can be evolutionarily traced to zebrafish. Using CRISPR-Cas12a knockout and rescue assays, we found that knocking out many human coPARSE-lncRNAs led to cell proliferation defects that were rescued by predicted zebrafish homologs. Knocking down the coPARSE-lncRNAs in zebrafish embryos caused severe developmental delays that were rescued by human homologs. Moreover, we verified that human, mouse, and zebrafish coPARSE-lncRNA homologs tend to bind similar RBPs with their conserved fuctions relying on specific RBP binding sites. Overall, our study demonstrates a comprehensive approach for studying functional conservation of lncRNAs and implicates numerous lncRNAs in regulating cellular physiology.

2024-01-26 | PXD046452 | Pride

Dicer-microRNA-Myc circuit promotes transcription of hundreds of long noncoding RNAs

Project description:Long noncoding RNAs (lncRNAs) are important regulators of cell fate, and their mis-expression has been implicated in many diseases. While distinct polymerases generate messenger vs. noncoding ribosomal or tRNAs3, little is known about distinct mechanisms controlling lncRNA expression. Here we show that transcription of lncRNAs is quantitatively different from that of messenger RNAs (mRNAs)--as revealed by deficiency of Dicer (Dcr), a key ribonuclease that generates microRNAs (miRNAs). Loss of Dcr in mouse embryonic stem cells (mESCs) led surprisingly to decreased level of the majority of lncRNAs. The canonical Dgcr8-Dcr-miRNA pathway is required for robust lncRNA expression, at the level of transcriptional initiation and elongation of lncRNA genes rather than at the level of their stability. cMyc, an oncogenic transcription factor, whose expression is indirectly regulated by Dcr-miRNA in mESCs, is partly responsible for lncRNA transcription. Loss of cMyc led to a more dramatic decrease of lncRNAs than mRNAs, and cMyc overexpression rescues lncRNA expression in Dcr KO cells. A quantitative metric of “mRNA-lncRNA decoupling” revealed that Dcr and cMyc differentially regulate lncRNAs vs. mRNAs in diverse cell types and in vivo, as evidenced by hundreds of microarray experiments. Thus, Dcr and cMyc may allow numerous lncRNAs to be activated or deactivated as a class, implicating lncRNAs to potential regulatory roles in development and disease states where Dcr and cMyc have been associated with. RNA was sequenced from WT and Dcr KO mESCs and the expression of lncRNAs and mRNAs are compared between WT and Dcr KO mESCs.

2014-06-15 | E-GEOD-55338 | biostudies-arrayexpress

Gene expression data from children diagnosed with ALL in vitro sensitive or resistant to prednisolone

Project description:Although the prognosis for childhood Acute Lymphoblastic Leukemia (ALL) in general has improved tremendously over the last decades, the survival chances for infants (<1 year of age) with ALL remains poor. A major obstacle hampering successful treatment results in infant ALL is cellular resistance to several drugs currently used in the treatment of ALL, especially to prednisolone (or prednisone). Therefore we set out to search for genes differentially expressed between from infant (children <1 year of age) and non-infant (children >1 year of age) ALL samples either resistant or sensitive to prednisolone. The in vitro prednisolone response in primary infant and non-infant ALL samples was determined by 4-day cytotoxicity (MTT) assays. Patient samples were characterized as either sensitive or resistant based on the LC50 value (i.e. the concentration of prednisolone lethal to 50% of the leukemic cells). Prednisolone sensitivity was defined by LC50 values <0.1 ug/mL prednisolone, and prednisolone resistance by LC50 values >150 ug/mL. Samples showing intermediate in vitro prednisolone responses were excluded. In total 25 infant (<1 year of age) and 27 non-infant (>1 year of age) ALL samples were selected for RNA extraction and hybridization on Affymetrix HU133A microarrays. The obtained gene expression signatures were used to identify gene differentially expressed between prednisolone resistant and sensitive patients, in order to gain insights into the mechanism(s) underlying prednisolone resistance in infant and non-infant ALL.

2009-12-15 | E-GEOD-19143 | biostudies-arrayexpress

Expression profiling of long noncoding RNAs and mRNAs in uterine leiomyoma

Project description:Global protein coding gene and miRNA expression profiling studies in uterine leiomyoma showed their aberrant expression and involvement in the pathogenesis of uterine leiomyoma. But the global expression patterns and potential clinical value of long noncoding RNA (lncRNA) in uterine leiomyoma have not been explored.In this study, we performed lncRNA expression profiles analysis of uterine leiomyoma using microarray(Arraystar Human LncRNA Array v2.0) to evaluate the genome-wide expression of lncRNAs and mRNAs and their potential role in the pathogenesis of uterine leiomyoma. Expression profiling analysis of the 15 samples including 5 large fibroids, 5 small fibroids and 5 matched myometrium by Arraystar Human LncRNA Array v2.0.

2014-08-14 | E-GEOD-52618 | biostudies-arrayexpress

Effect of emodin on long non-coding RNA-mRNA networks in rats with severe acute pancreatitis-induced acute lung injury

Project description:Long non-coding RNAs (lncRNAs) reportedly contribute to disease pathogenesis and drug treatment effects. Both emodin and dexamethasone (DEX) have been used for the treatment of severe acute pancreatitis-associated acute lung injury (SAP-ALI). However, lncRNA regulation networks related to SAP-ALI pathogenesis and drug treatment are unreported. In this study, lncRNAs and mRNAs in the lung tissue of SAP-ALI and control rats, with or without drug treatment (emodin or DEX), were assessed by RNA sequencing. Results showed that both emodin and DEX were therapeutic for SAP-ALI and that mRNA and lncRNA levels differed between untreated and treated SAP-ALI rats. Gene expression profile relationships for emodin treated and control rats were higher than DEX treated and untreated animals. By comparison of control and SAP-ALI animals, more upregulated than downregulated mRNAs and lncRNAs were observed with emodin treatment. For DEX treatment, more downregulated than upregulated mRNAs and lncRNAs were observed. Functional analysis demonstrated both upregulated mRNA and co-expressed genes with upregulated lncRNAs were enriched in inflammatory and immune response pathways. Further, emodin associated lncRNAs and mRNAs co-expressed modules were different from those associated with DEX. Quantitative polymerase chain reaction demonstrates that selected lncRNA and mRNA co-expressed modules were different in the lung tissue of emodin and DEX treated rats. Also, emodin had different effects compared to DEX on the co-expression network of lncRNAs Rn60_7_1164.1 and AABR07062477.2 for the blue lncRNA module and Nrp1 for the green mRNA module. In conclusion, this study provides evidence that emodin may be a suitable alternative or complementary medicine for treatment of SAP-ALI.

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