Clinical significance of microRNAs in chronic and acute human leukemia

Yeh, Chien‐Hung; Moles, Ramona; Nicot, Christophe

doi:10.1186/s12943-016-0518-2

Cited by 127 publications

(123 citation statements)

References 181 publications

(228 reference statements)

Supporting

Mentioning

119

Contrasting

Unclassified

Order By: Relevance

“…Physiologically, it is involved in hematopoiesis, immunity, and inflammatory processes . Also, it is involved in the pathogenesis of malignancies and heart and renal diseases . miRNAs have a critical role in viral infections, and one of them is hepatitis C virus (HCV) infection.…”

Section: Introductionmentioning

confidence: 99%

In vitro knock‐out of miR‐155 suppresses leukemic and HCV virus loads in pediatric HCV‐4–associated acute lymphoid leukemia: A promising target therapy

Hassan

El-Khazragy⃰

Elshimy

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Hepatitis C virus (HCV) infection is a major public health problem, having a high prevalence in Egypt. Leukemia and lymphoma have been associated with HCV infection. MicroRNA‐155 (miR‐155) has been reported to play a regulatory role in cancer, inflammation, and immune response to infection. The expression level of miR‐155 in HCV viremic patients is controversial; although high miR‐155 levels were demonstrated in HCV genotypes 1,2, and 3, low levels of miR‐155 were detected in Egyptian patients with HCV genotype 4. Several studies have investigated the correlation between the levels of miRNA‐155 and the replication of HCV, others have evaluated miRNA‐155 as a prognostic biomarker in different types of cancer. No studies have investigated the impact of miRNA‐155 knockdown on HCV pediatric patients associated with childhood acute lymphoblastic leukemia (ALL). We knocked‐out the miR_155a in cultured polymorphonuclear cells (PBMCs) obtained from 60 children with ALL; 30 were associated with HCV‐4 infection and 30 were HCV negative. The miR_155a, HCV viral load, and cell proliferation werre assessed in treated and untreated cells using TaqMan assay quantitative polymerase chain reaction. We found that miRNA‐155 was significantly upregulated by seven folds in the HCV‐4 associated ALL group; while being linked to high HCV viral load and leukemic burden, miR_155a knock‐out can improve the disease outcome. We conclude that miR‐155 is a critical miRNA that is considered a therapeutic target in pediatric HCV leukemic patients.

show abstract

Section: Introductionmentioning

confidence: 99%

In vitro knock‐out of miR‐155 suppresses leukemic and HCV virus loads in pediatric HCV‐4–associated acute lymphoid leukemia: A promising target therapy

Hassan

El-Khazragy⃰

Elshimy

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…In the disease context such as in cancer, alterations of miRNA expression are common and specific miRNA deregulation profiles are sufficient to distinguish cancerous from non-cancerous tissues and to predict invasiveness and aggressiveness of various cancers [24][25][26]. The widespread miRNA deregulation in cancers has been attributed to genomic copy number changes.…”

Section: Introductionmentioning

confidence: 99%

The deregulated microRNAome contributes to the cellular response to aneuploidy

et al. 2018

View full text Add to dashboard Cite

Background: Aneuploidy, or abnormal chromosome numbers, severely alters cell physiology and is widespread in cancers and other pathologies. Using model cell lines engineered to carry one or more extra chromosomes, it has been demonstrated that aneuploidy per se impairs proliferation, leads to proteotoxic as well as replication stress and triggers conserved transcriptome and proteome changes. Results: In this study, we analysed for the first time miRNAs and demonstrate that their expression is altered in response to chromosome gain. The miRNA deregulation is independent of the identity of the extra chromosome and specific to individual cell lines. By cross-omics analysis we demonstrate that although the deregulated miRNAs differ among individual aneuploid cell lines, their known targets are predominantly associated with cell development, growth and proliferation, pathways known to be inhibited in response to chromosome gain. Indeed, we show that up to 72% of these targets are downregulated and the associated miRNAs are overexpressed in aneuploid cells, suggesting that the miRNA changes contribute to the global transcription changes triggered by aneuploidy. We identified hsa-miR-10a-5p to be overexpressed in majority of aneuploid cells. Hsa-miR-10a-5p enhances translation of a subset of mRNAs that contain so called 5'TOP motif and we show that its upregulation in aneuploids provides resistance to starvation-induced shut down of ribosomal protein translation.

show abstract

“…A miRNA may function as a tumour suppressor or an oncogene (15). An example of this is hsa-miR-17/92, which has been shown to target BCL2, STAT5 and JAK2 (tumour suppressor), as well as the CDK inhibitor CDKN1A (p21), functioning as an oncogene.…”

Section: Introductionmentioning

confidence: 99%

“…This cluster of miRNAs also exhibits increased expression in the early chronic phase of CML, but not in blast phase (BP), making it a possible therapeutic target. Downregulation of hsa-miR-328 has also been described as a crucial stage of disease progression to BP (15).…”

Section: Introductionmentioning

confidence: 99%

Preliminary data on microRNA expression profiles in a group of South African patients diagnosed with chronic myeloid leukaemia

Prinsloo

Pool

Niekerk

2017

Molecular and Clinical Oncology

View full text Add to dashboard Cite

Abstract. Micro-ribonucleic acids (miRNAs) are small functional non-coding RNAs that downregulate gene expression at the post-transcriptional level. Abnormal expression of specific miRNAs has been recorded in chronic lymphocytic leukaemia, other non-Hodgkin B-cell lymphomas, lung cancer and chronic myeloid leukaemia (CML). The aim of this study was to compare miRNA expression profiles among patients with newly diagnosed CML, those on established therapy with imatinib mesylate, and healthy individuals. The expression of 88 miRNAs was evaluated in a total of nine samples divided into three groups: Group 1 comprised three samples collected from newly diagnosed CML patients; group 2 consisted of three samples collected from patients on therapy; the remaining three samples were collected from healthy volunteers (control group). Total RNA was extracted from whole blood and reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) was performed on the LightCycler ® 480 platform using Human Serum & Plasma miRNA PCR Arrays. In group 1, only SNORD44 was downregulated, while hsa-miR-372 and hsa-miR-375 were found to be significantly upregulated compared with the control group. By contrast, 49 miRNAs were significantly upregulated in group 2 compared with the control group. miRNAs hsa-miR-106b, hsa-miR-21, hsa-miR-221, hsa-miR-10a, hsa-miR-193a-5p and hsa-miR-30e were expressed in group 2. Therefore, miRNA expression profiles differed between the two patient groups. IntroductionChronic myeloid leukaemia (CML) is an acquired disease resulting from the malignant transformation of a single stem cell, characterized by anaemia extreme blood granulocytosis and granulocytic immaturity (1). CML is triggered by a reciprocal translocation of the long arms of chromosomes 9 and 22, referred to as the Philadelphia chromosome (2). The breakpoint cluster region (BCR) gene on chromosome 22 and the Abelson murine leukaemia viral oncogene homolog 1 (ABL1) gene on chromosome 9 are involved in this t(9;22)(q34;q11) translocation leading to the formation of a new chimeric fusion oncogene, BCR-ABL1. Expression of this fusion oncogene produces an abnormal, elongated 8-kb ribonucleic acid (RNA) fragment, which is translated into a unique tyrosine phosphoprotein kinase, considered to be essential for the development of the leukaemic phenotype (1,3).Imatinib mesylate (Gleevec ® ; Novartis, Basel, Switzerland) has been established as the standard first-line therapy for CML (4,5). Response to therapy is defined as optimal, suboptimal, or failure of treatment. Optimal response is defined as follows: Complete haematological response [normal full blood count, minimal cytogenetic response (CyR) at 3 months]; partial cytogenetic response at 6 months; complete CyR (CCyR) at 12 months and major molecular response (≥3-log reduction in BCR-ABL1 transcripts) at 18 months (6).MicroRNAs (miRNAs) have recently been identified as a class of small functional non-coding RNAs of 18-25 nucleotides (7,8) which bind to the 3'-untranslated region of mRNAs, do...

show abstract

Clinical significance of microRNAs in chronic and acute human leukemia

Cited by 127 publications

References 181 publications

In vitro knock‐out of miR‐155 suppresses leukemic and HCV virus loads in pediatric HCV‐4–associated acute lymphoid leukemia: A promising target therapy

In vitro knock‐out of miR‐155 suppresses leukemic and HCV virus loads in pediatric HCV‐4–associated acute lymphoid leukemia: A promising target therapy

The deregulated microRNAome contributes to the cellular response to aneuploidy

Preliminary data on microRNA expression profiles in a group of South African patients diagnosed with chronic myeloid leukaemia

Contact Info

Product

Resources

About