MicroRNAs in acute leukemia: from biological players to clinical contributors

Schotte, Diana; Pieters, Rob; Boer, Monique L. den

doi:10.1038/leu.2011.151

Cited by 123 publications

(106 citation statements)

References 101 publications

(188 reference statements)

Supporting

Mentioning

102

Contrasting

Unclassified

Order By: Relevance

“…Through their oncogenic or tumor-suppressive function, they are involved in oncogenesis of solid and blood cancers. [26][27][28][29] MiRNAs also play important role in the chromatin structure control by regulation at the post-transcriptional level of the chromatin modifying enzymes including PcG subunits.…”

Section: Micrornas Biologymentioning

confidence: 99%

Non‐coding RNAs and EZH2 interactions in cancer: Long and short tales from the transcriptome

Benetatos¹,

Voulgaris

Vartholomatos

et al. 2012

Intl Journal of Cancer

View full text Add to dashboard Cite

A large amount of data indicates that non‐coding RNAs represent more than the “dark matter” of the genome. Both microRNAs and long non‐coding RNAs are involved in several fundamental biologic processes, and their deregulation may lead in oncogenesis. Interacting with the Polycomb‐repressive complex 2 subunit EZH2, they could affect the expression of protein‐coding genes and form feedback networks and autoregulatory loops. They can also form networks with upstream and downstream important factors, in which EZH2 represent the stabilizing factor of the pathway. As such non‐coding RNAs affect the epigenetic modifications leading to malignant transformation.

show abstract

Section: Micrornas Biologymentioning

confidence: 99%

Non‐coding RNAs and EZH2 interactions in cancer: Long and short tales from the transcriptome

Benetatos¹,

Voulgaris

Vartholomatos

et al. 2012

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Biological players that have been studied for clinical applications include deacetylases [32,[105][106][107][108], DNA and histone methyltransferases [32,35,103,104,[109][110][111][112][113][114][115][116][117][118][119][120][121][122][123][124][125] and miRNA [104,119,126,127]. Besides APL and AML, further data have been collected for leukaemogenesis, including transforming factors and epigenetic alterations [106,111,[128][129][130][131].…”

Section: Hematological Malignanciesmentioning

confidence: 99%

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Andreoli¹,

Barbosa²,

Parenti³

et al. 2012

CPD

View full text Add to dashboard Cite

Abstract:Research on cancer epigenetics has flourished in the last decade. Nevertheless growing evidence point on the importance to understand the mechanisms by which epigenetic changes regulate the genesis and progression of cancer growth. Several epigenetic targets have been discovered and are currently under validation for new anticancer therapies. Drug discovery approaches aiming to target these epigenetic enzymes with small-molecules inhibitors have produced the first pre-clinical and clinical outcomes and many other compounds are now entering the pipeline as new candidate epidrugs. The most studied targets can be ascribed to histone deacetylases and DNA methyltransferases, although several other classes of enzymes are able to operate post-translational modifications to histone tails are also likely to represent new frontiers for therapeutic interventions. By acknowledging that the field of cancer epigenetics is evolving with an impressive rate of new findings, with this review we aim to provide a current overview of pre-clinical applications of smallmolecules for cancer pathologies, combining them with the current knowledge of epigenetic targets in terms of available structural data and drug design perspectives.Keywords: Epigenetics, anticancer therapy, DNA methyltransferases, protein methyltransferases, demethylases, deacetylases, acetyltransferases, histone post-translational modifications, drug design, crystallography, small-molecule inhibitors. INTRODUCTIONThe term epigenetics currently refers to the mechanisms of temporal and spatial control of gene activity that do not depend on the DNA sequence, influencing the physiological and pathological development of an organism. The molecular mechanisms by which epigenetic changes occur are complex and cover a wide range of processes including paramutation, bookmarking, imprinting, gene silencing, carcinogenesis progression, and, most importantly, regulation of heterochromatin and histone modifications [1]. At a biochemical level, epigenetic alterations in chromatin involve methylation of DNA patterns, several forms of histone modifications and microRNA (miRNA) expression. All these processes modulate the structure of chromatin leading to the activation or silencing of gene expression [2][3][4][5][6]. More specifically, the chromatin remodeling is accomplished by two main mechanisms that concern the methylation of cytosine residues in DNA and a variety of post-translational modifications (PTMs) occurring at the N-terminal tails of histone proteins. These PTMs include acetylation, methylation, phosphorylation, ubiquitylation, sumoylation, glycosylation, ADPribosylation, carbonylation, citrullination and biotinylation [7,8]. Among all PTMs for example, histone tails can have its lysine residues acetylated, methylated or ubiquitilated; arginine can be methylated; serine and threonine residues can be phosphorylated [9][10][11][12][13][14][15][16][17]. These covalent modifications are able to cause other PTMs and the ensemble of this cross-talk is known as the his...

show abstract

“…This outcome indicates that miR-301a is involved in the pathogenesis of OS. miRNAs can act as oncogenes or tumor suppressors, and are involved in numerous cellular processes, playing roles in tumorigenesis by regulating cell differentiation, cell proliferation, and the cell cycle (Song and Ju, 2010;Rottiers et al, 2011;Sandoval and Esteller, 2012;Schotte et al, 2012). miR-301a has also been shown to have a cancerous function in several human tumors, such as pancreatic, prostate, colorectal, and breast cancers (Ma et al, 2014;Zhang et al, 2014;Xia et al, 2015;Xie et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

Wang

et al. 2016

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. MicroRNAs (miRs) are associated with tumor progression in various cancers, such as gastric and hepatic carcinomas, and lung cancer. miR-301a is overexpressed and displays oncogenic activity in cancers. We investigated the biological involvement of miR301a in osteosarcoma (OS). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze expression levels of miR-301a in 24 OS and matched adjacent non-tumor tissues. A miR-301a mimic was transferred into OS cell lines U-2 OS and MG-63 to upregulate miR-301a. The effects of miR-301a were investigated by examining cell proliferation, migration, and the cell cycle. The miR-301 target was predicted by TargetScan and confirmed by western blotting and qRT-PCR. The expression of miR-301a was significantly higher in OS tissues compared with the matched adjacent non-tumor tissues (0.959 ± 0.39 vs 3.9516 ± 1.18). Upregulated miR-301a significantly increased proliferation at 48 and 72 h compared to the negative control (U-2 OS: 2.11 ± 0.21 vs 2.88 ± 0.24; 2.70 ± 0.26 vs 3.71 ± 0.24; MG-63: 2.19 ± 0.20 vs 3.19 ± 0.22; 3.1 ± 0.25 vs 4.01 ± 0.27) and migration capability (U-2 OS: 100 ± 20.19 vs 150.68 ± 32.83; MG-63: 100 ± 17.20 vs 133.35 ± 26.26), and decreased apoptosis in both U-2 OS (10.87 ± 2.53 vs 4.01 ± 2.23) and MG-63 (15.26 ± 2.15 vs 8.25 ± 3.07). The cell cycle studies revealed that miR-301a caused an increase of the G2 population in U-2 OS (38.6 ± 6.58 vs 47.2 ± 7.27) and . Additional experiments indicated that CDC14A was upregulated by miR-301a (0.63 ± 0.06 vs 0.98 ± 0.06; 1.49 ± 0.25 vs 2.99 ± 0.14). Overexpressed miR-301a may increase CDC14A expression and promote cell proliferation and migration in OS cells. Therefore, miR301a may be useful for osteosarcoma diagnosis and therapy.

show abstract

MicroRNAs in acute leukemia: from biological players to clinical contributors

Cited by 123 publications

References 101 publications

Non‐coding RNAs and EZH2 interactions in cancer: Long and short tales from the transcriptome

Non‐coding RNAs and EZH2 interactions in cancer: Long and short tales from the transcriptome

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

Contact Info

Product

Resources

About