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

Benetatos, Leonidas; Voulgaris, E.; Vartholomatos, George; Hatzimichael, Eleftheria

doi:10.1002/ijc.27859

Cited by 70 publications

(70 citation statements)

References 96 publications

(99 reference statements)

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“…Several miRNA negatively regulate EZH2 expression, for example, miRNA-101, miRNA-26a, miR-29, and miR-214 negatively regulate EZH2 during various differentiation processes. 56 Furthermore, downregulation of miRNA is frequently associated with abnormally elevated levels of EZH2 in cancer; for instance, the downregulation of miR-25 and miR30d is involved in thyroid carcinoma 57 , let-7 in prostate cancer, 58 miR-98 and miR-214 in esophageal squamous cell carcinoma, miR26a and miR-29 in rhabdomyosarcoma. 59,60 Post-translational modifications of EZH2 PRC2 activity can be regulated by post-translational modifications that are able to control the recruitment of target genes and/or its catalytic activity.…”

Section: Transcriptional Regulation Of Prc2mentioning

confidence: 99%

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

Marchesi

Giordano

Bagella³

2014

Cell Cycle

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Section: Transcriptional Regulation Of Prc2mentioning

confidence: 99%

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

Marchesi

Giordano

Bagella³

2014

Cell Cycle

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“…Also c-Myc binds EZH2 promoter and induces transcription through the acetylation of histones H3 and H4 [91] . Furthermore, several miRNA are also involved in EZH2 regulation [92] . It has been discovered that a natural compound isolated from the bark of Polyalthia longifolia, 16-Hydroxycleroda-3,13-dien-15,16-olide (PL3), induces apoptosis in leukemia cells [93] .…”

Section: Marchesi I Et Al Ezh2 Inhibitors In Cancer Therapymentioning

confidence: 99%

Targeting Enhancer of Zeste Homolog 2 as a promising strategy for cancer treatment

Marchesi

Bagella

2016

WJCO

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Polycomb group proteins represent a global silencing system involved in development regulation. In specific, they regulate the transition from proliferation to differentiation, contributing to stem-cell maintenance and inhibiting an inappropriate activation of differentiation programs. Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb repressive complex 2, which induces transcriptional inhibition through the tri-methylation of histone H3, an epigenetic change associated with gene silencing. EZH2 expression is high in precursor cells while its level decreases in differentiated cells. EZH2 is upregulated in various cancers with high levels associated with metastatic cancer and poor prognosis. Indeed, aberrant expression of EZH2 causes the inhibition of several tumor suppressors and differentiation genes, resulting in an uncontrolled proliferation and tumor formation. This editorial explores the role of Polycomb repressive complex 2 in cancer, focusing in particular on EZH2. The canonical function of EZH2 in gene silencing, the non-canonical activities as the methylation of other proteins and the role in gene transcriptional activation, were summarized. Moreover, mutations of EZH2, responsible for an increased methyltransferase activity in cancer, were recapitulated. Finally, various drugs able to inhibit EZH2 with different mechanism were described, specifically underscoring the effects in several cancers, in order to clarify the role of EZH2 and understand if EZH2 blockade could be a new strategy for developing specific therapies or a way to increase sensitivity of cancer cells to standard therapies.

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“…EZH2 encodes enzymatic component of the polycomb repressive complex2, which is a Histone 3 Lysine 27 (H3K27) methyltransferase, controls stem cell renewal by epigenetic alteration [156]. Over-expression of EZH2 has been described in both solid tumors and leukemia [157] and has been shown to be caused by the removal of transcriptional repression of specific microRNAs [157]. In myeloid neoplasms, mutations were found throughout the EZH2 and have been described in 10-13% of poor-prognosis MDS or MPN 13% of myelofibrosis , and 6% of MDS [158,159].…”

Section: Ezh2 Mutationsmentioning

confidence: 99%

Distinct Gene Mutations, their Prognostic Relevance and Molecularly Targeted Therapies in Acute Myeloid Leukemia (AML)

Tayyab¹

2014

J Cancer Sci Ther

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Acquired genetic alterations which include balanced and unbalanced chromosome aberrations and submicroscopic gene mutations and changes in gene expression strongly influenced by pretreatment clinical features and prognosis of adults patients with acute myeloid leukemia (AML). Cytogenetic profiling separate AML patients into three broad prognostic groups: favorable, intermediate and adverse. The cytogenetic risk classifications vary to some extent for younger adult patients and for those aged 60 years or older. In many cases, patients with specific cytogenetic rearrangement such as those with a normal karyotype or those with either RUNX1-RUNX1T1 or CBFB-MYH11 feature of core-binding factor (CBF) can be further subdivided into prognostic categories depend on the presence or absence of specific gene mutations or changes in gene expression. Advancement in the understanding of cancer genetic and discovery of recurrent mutations in AML provide opportunity to develop targeted therapies and improve the clinical outcome. The identified gene mutations, mainly targetable lesions are gain of function mutations of JAK2 and cKIT and FLT3 in APL have been associated with clinical features and/ or outcome of patients with these AML subtypes. These data emphasize the significance of genetic testing for common translocations for diagnosis, prognosis and increasingly targeted therapy in acute leukemia. Notably, these several molecular genetic alterations constitute a variety of diverse new targets for salvage therapies. These approaches intend to develop targeted treatment concepts that depend on interference with molecular genetics or epigenetic mechanisms. This report provides an overview on characteristic gene mutations, discuss their biological functions and Prognostic significance, which serve as basis for selected therapy approaches now or might represent options for such approaches in the future and expected to have a role in treating AML subtypes with characteristic molecular alterations.

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

Cited by 70 publications

References 96 publications

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

Targeting Enhancer of Zeste Homolog 2 as a promising strategy for cancer treatment

Distinct Gene Mutations, their Prognostic Relevance and Molecularly Targeted Therapies in Acute Myeloid Leukemia (AML)

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