RNA and transcriptional modulation of gene expression

Hawkins, Peter G.; Morris, Kevin V.

doi:10.4161/cc.7.5.5522

Cited by 128 publications

(93 citation statements)

References 68 publications

(85 reference statements)

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“…miRNAs are involved in a variety of basic physiological and pathological processes, including cell proliferation, differentiation, metabolism and apoptosis (9,10). Previous studies have demonstrated that miRNAs are frequently downregulated or dysregulated in a range of types of malignancy, including ICC, breast cancer and colorectal cancer, potentially acting as oncogenes or tumor suppressor genes (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-26b-5p regulates cell proliferation, invasion and metastasis in human intrahepatic cholangiocarcinoma by targeting S100A7

Fan

et al. 2017

Oncol Lett

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Abstract. The present study aimed to investigate the effects of microRNA expression in intrahepatic cholangiocarcinoma (ICC). It was identified that the expression of microRNA-26b-5p (miR-26b-5p) was downregulated in ICC tissues compared with matched adjacent non-tumor tissues. Furthermore, miR-26b-5p expression was downregulated in metastatic ICC tumor tissues and invasive ICC cell line subpopulations compared with non-metastatic tumor tissue and the parental ICC cells. In vitro studies demonstrated that transfection with an miR-26b-5p mimic inhibited the proliferation, migration and invasion of RBE and HCCC-9810 cells, whereas an miR-26b-5p inhibitor promoted these abilities. S100 calcium-binding protein A7 (S100A7) was predicted as a direct target of miR-26b-5p. Transfection with an miR-26b-5p mimic decreased S100A7 expression, whereas an miR-26b-5p inhibitor increased S100A7 expression. The result of a dual luciferase reporter assay also indicated this interaction. S100A7 was therefore confirmed as a direct target of miR-26b-5p in ICC. The knockdown of S100A7 abrogated the effect of miR-26b-5p on cell migration in RBE and HCCC-9810 cells. In conclusion, the present study demonstrated that miR-26b-5p suppresses the proliferation, migration and invasion of ICC cells by suppressing S100A7.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-26b-5p regulates cell proliferation, invasion and metastasis in human intrahepatic cholangiocarcinoma by targeting S100A7

Fan

et al. 2017

Oncol Lett

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“…Also, HDAC inhibition by TSA up-regulated a similar set of genes, possibly delineating EZH2 ability to interact with HDAC2 via the EED protein (11). Emerging data suggest that noncoding RNA might be guiding chromatin modifying complexes to epigenetically silenced target genes (16,30). To test the relevance of this approach, we suppressed AGO1 that is necessary for this process (31).…”

Section: Discussionmentioning

confidence: 99%

“…Several mechanisms, including direct recruitment of the PRC2 complex to the promoters of genes, could be relevant for the regulation of these genes. Recently, it has been suggested that noncoding RNAs may direct transcriptional coregulators to their site of action (16). To test this approach, we silenced Argonaute-1 (AGO1), and subsequently observed down-regulation of NGFR expression, but no regulation of EPHB2, EMP1, or GAP43 (Fig.…”

Section: Blockade Of Hdac and Ezh2 Increases The Expression Of Genesmentioning

confidence: 99%

EZH2 is a mediator of EWS/FLI1 driven tumor growth and metastasis blocking endothelial and neuro-ectodermal differentiation

Plehm¹,

Fasan²,

Rössler³

et al. 2009

Klin Padiatr

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Ewing tumors (ET) are highly malignant, localized in bone or soft tissue, and are molecularly defined by ews/ets translocations. DNA microarray analysis revealed a relationship of ET to both endothelium and fetal neural crest. We identified expression of histone methyltransferase enhancer of Zeste, Drosophila, Homolog 2 (EZH2) to be increased in ET. Suppressive activity of EZH2 maintains stemness in normal and malignant cells. Here, we found EWS/FLI1 bound to the EZH2 promoter in vivo, and induced EZH2 expression in ET and mesenchymal stem cells. Down-regulation of EZH2 by RNA interference in ET suppressed oncogenic transformation by inhibiting clonogenicity in vitro. Similarly, tumor development and metastasis was suppressed in immunodeficient Rag2 ؊/؊ ␥C ؊/؊ mice. EZH2-mediated gene silencing was shown to be dependent on histone deacetylase (HDAC) activity. Subsequent microarray analysis of EZH2 knock down, HDAC-inhibitor treatment and confirmation in independent assays revealed an undifferentiated phenotype maintained by EZH2 in ET. EZH2 regulated stemness genes such as nerve growth factor receptor (NGFR), as well as genes involved in neuroectodermal and endothelial differentiation (EMP1, EPHB2, GFAP, and GAP43). These data suggest that EZH2 might have a central role in ET pathology by shaping the oncogenicity and stem cell phenotype of this tumor.epigenetic regulation ͉ Ewing tumor ͉ stemness E wing tumors (ET) are highly malignant tumors with an approximate incidence of 3.3/10 6 in children under the age of 15. ET are characterized by early metastases, and metastatic spread is commonly hematogeneous. ET were originally described by Ewing in 1921 as endothelioma of the bone (1), and we confirmed this endothelial signature by microarray analysis (2). ET are molecularly defined by ews/ets translocations. Translocation-derived chimeric transcription factors yield transactivation, transformation, and the highly malignant phenotype. In mice, EWS/FLI1 transforms bone marrow derived or mesenchymal progenitor cells, and generates tumors (3, 4), which have features of ET. Also, inhibition of EWS/FLI1 expression may allow ET cells to recover the phenotype of their presumed mesenchymal stem cell (MSC) progenitor (5). Multipotent MSCs represent a leading candidate for primary transformation in ET. We revealed a relationship of ET to both endothelial and fetal neural crest-derived cells (2), after having demonstrated neuroectodermal histogenesis of ET in 1985 (6). Based on our recent study, we postulated in 2004 that the ET stem cell is arrested at early mesenchyme development from the neuroectodermal germ layer, and, thus, the ET stem cell is a neuronal crest-derived stem cell at transition to mesenchymal endothelial development, residing in the bone marrow. However, ectopic EWS/FLI1 expression resulted in a neural phenotype, raising the possibility that transdifferentiation or lineage promiscuity may be an alternative to the MSC histogenetic origin hypothesis of ET (7).We used high density DNA microarrays for the ident...

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“…They are associated with the RNA-induced silencing complex through partly complementary sequences localized in the 3′ untranslated region of the mRNA target [27]. Moreover, some miRNAs occasionally induce changes in chromatin structure of the targeted promoter, e.g., by decreasing active-state histone modifications, or increasing histone methylation marks and DNA methylation [28]. Recent studies have shown significant polymorphisms in miRNAs.…”

Section: Mirna Biologymentioning

confidence: 99%

Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

Zhang

Dong

Yang

2011

Sci. China Life Sci.

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Atrial fibrillation (AF) remains one of the leading causes of morbidity and mortality in the world which are related to palpitations, fainting, congestive heart failure or stroke. The mechanism for atrial fibrillation has been identified as electrical remodeling, structure remodeling and intracellular calcium handling remodeling. microRNAs (miRNAs) have recently emerged as one of the important factors in regulating gene expression. So far, thousands of miRNA genes have been found in diverse animals with the function of regulating cell death, cell proliferation, haematopoiesis and even participate in the processing of cardiovascular disease. In this review, we summarize the mechanism of AF and the association of microRNAs network with AF. We provide a potential perspective of miRNAs as the therapeutic target for AF. atrial fibrillation, remodeling, microRNA Citation:Zhang Y, Dong D L, Yang B F. Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation.

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RNA and transcriptional modulation of gene expression

Cited by 128 publications

References 68 publications

MicroRNA-26b-5p regulates cell proliferation, invasion and metastasis in human intrahepatic cholangiocarcinoma by targeting S100A7

MicroRNA-26b-5p regulates cell proliferation, invasion and metastasis in human intrahepatic cholangiocarcinoma by targeting S100A7

EZH2 is a mediator of EWS/FLI1 driven tumor growth and metastasis blocking endothelial and neuro-ectodermal differentiation

Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

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