Characterization of the uterine leiomyoma microRNAome by deep sequencing

Georgieva, Boryana; Milev, Ivan; Minkov, Ivan; Dimitrova, Irina; Bradford, Andrew P.; Baev, Vesselin

doi:10.1016/j.ygeno.2012.03.003

Cited by 69 publications

(51 citation statements)

References 43 publications

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“…Overexpression of miR-217 can reverse the malignant behavior of pancreatic ductal adenocarcinoma cells. miR-217 is also found to be one of the top five significantly de-regulated miRNAs in human uterine leiomyoma (ULM) [9].These studies provide evidences for the important function of miR-217 in the pathogenesis of human diseases. However, its role in ccRCC remains largely unknown.…”

Section: Discussionmentioning

confidence: 63%

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MicroRNA-217, down-regulated in clear cell renal cell carcinoma and associated with lower survival, suppresses cell proliferation and migration

Zhao²,

Zhang³

et al. 2013

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Aberrantly expressed microRNAs (miRNAs) are frequently correlated with a variety of human cancers, including clear cell renal cell carcinoma (ccRCC). In this study, we determined the expression patterns of miR-217 in ccRCC, and tested its effect on cancer cell proliferation and migration. The expression levels of miR-217 were determined in 54 ccRCC samples using Real-Time qPCR. 786-O and ACHN cells were transfected with miR-217 mimics or miRNA mimics control. Cell proliferation and migration were evaluated by MTT assay and scratch-wound assay, respectively. We found that miR-217 was down-regulated in ccRCC compared to paired normal tissue. Lower miR-217 expression levels were associated with higher tumor grade and stage. All patients with high miR-217 expression survived 5 years, while with low miR-217 expression, only 40% survived. Cell proliferation inhibition and decreased motility were observed in cells transfected with the miR-217 mimics. In conclusion, miR-217 plays a tumor suppressor role in ccRCC.

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Section: Discussionmentioning

confidence: 63%

“…As a potential tumor suppressor, miR-217 has been shown to be aberrantly expressed in several types of tumors, such as pancreatic ductal adenocarcinoma [8] and uterine leiomyoma [9]. Previous work has also demonstrated that miR-217 can down-regulate the tumor suppressor gene PTEN in kidney disorders [10].…”

mentioning

confidence: 99%

MicroRNA-217, down-regulated in clear cell renal cell carcinoma and associated with lower survival, suppresses cell proliferation and migration

Zhao²,

Zhang³

et al. 2013

neo

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“…Two small RNA libraries of BT474 CSC, and MDA-MB-468 CSC were established by following the described methods [29]. We filtered the low quality reads according to base quality value.…”

Section: Rna Extraction Construction and Solexa Sequencing Of Small mentioning

confidence: 99%

MiR-4319 Suppress the Malignancy of Triple-Negative Breast Cancer by Regulating Self-Renewal and Tumorigenesis of Stem Cells

Chu

Fan

et al. 2018

Cell Physiol Biochem

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Background/Aims: High levels of cancer stem cells (CSCs) in patients with triple-negative breast cancer (TNBC) correlate with risk of poor clinical outcome and possibly contribute to chemoresistance and metastasis in patients with highly malignant TNBC. Aberrant microRNA expression is associated with the dysfunction of self-renewal and proliferation in cancer stem cells, while there is little information about the TNBC-specific microRNAs in regulating CSC ability. Methods: Solexa deep sequencing was performed to detect the expression levels of TNBC or non-TNBC stem cells (CSCs) microRNAs. Mammosphere formation assay, qRT-PCR and the xenograft model in nude mice were performed. Bioinformatic analysis and microarray were used to select the target gene, and luciferase reporter assays were used to confirm the binding sites. Results: Solexa sequencing data exhibited differential expression of 193 microRNAs between TNBC and non-TNBC stem cells. The gene ontology analysis and pathways analyses showed that genes were involved in the maintenance of stemness. MiR-4319 could suppress the self-renewal and formation of tumorspheres in TNBC CSCs through E2F2, and also inhibited tumor initiation and metastasis in vivo. Moreover, increased E2F2 could reverse the effect of miR-4319 on the self-renewal in TNBC CSCs. Conclusions: MiR-4319 suppresses the malignancy of TNBC by regulating self-renewal and tumorigenesis of stem cells and might be a remarkable prognostic factor or therapeutic target for patients with TNBC.

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“…A number of studies have been conducted to perform profiling and function analyses of miRNAs in human uterine leiomyoma using microarray and deep sequencing. 82,[127][128][129] These studies demonstrate that many miRNAs regulating cellular processes including cell proliferation, apoptosis, cell adhesion, WNT signaling, mitogen-activated protein kinase (MAPK) signaling, nuclear factor kB (NF-kB) activation, and insulin signaling are deregulated in leiomyoma when compared to normal tissues. Importantly, the predicted targets of these deregulated miRNAs including let-7, miR-21, miR-23b, miR-29b, and miR-197 in leiomyoma play an important role in the pathogenesis of leiomyoma.…”

Section: Dysregulation Of Mirna In Uterine Leiomyomamentioning

confidence: 99%

The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development

et al. 2016

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Uterine leiomyomas, also known as uterine fibroids, are the most common pelvic tumors, occurring in nearly 70% of all reproductive-aged women and are the leading indication for hysterectomy worldwide. The development of uterine leiomyomas involve a complex and heterogeneous constellation of hormones, growth factors, stem cells, genetic, and epigenetic abnormalities. An increasing body of evidence emphasizes the important contribution of epigenetics in the pathogenesis of leiomyomas. Genome-wide methylation analysis demonstrates that a subset of estrogen receptor (ER) response genes exhibit abnormal hypermethylation levels that are inversely correlated with their RNA expression. Several tumor suppressor genes, including Kruppel-like factor 11 (KLF11), deleted in lung and esophageal cancer 1 (DLEC1), keratin 19 (KRT19), and death-associated protein kinase 1 (DAPK1) also display higher hypermethylation levels in leiomyomas when compared to adjacent normal tissues. The important role of active DNA demethylation was recently identified with regard to the ten-eleven translocation protein 1 and teneleven translocation protein 3-mediated elevated levels of 5-hydroxymethylcytosine in leiomyoma. In addition, both histone deacetylase and histone methyltransferase are reported to be involved in the biology of leiomyomas. A number of deregulated microRNAs have been identified in leiomyomas, leading to an altered expression of their targets. More recently, the existence of side population (SP) cells with characteristics of tumor-initiating cells have been characterized in leiomyomas. These SP cells exhibit a tumorigenic capacity in immunodeficient mice when exposed to 17b-estradiol and progesterone, giving rise to fibroid-like tissue in vivo. These new findings will likely enhance our understanding of the crucial role epigenetics plays in the pathogenesis of uterine leiomyomas as well as point the way to novel therapeutic options.

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Characterization of the uterine leiomyoma microRNAome by deep sequencing

Cited by 69 publications

References 43 publications

MicroRNA-217, down-regulated in clear cell renal cell carcinoma and associated with lower survival, suppresses cell proliferation and migration

MicroRNA-217, down-regulated in clear cell renal cell carcinoma and associated with lower survival, suppresses cell proliferation and migration

MiR-4319 Suppress the Malignancy of Triple-Negative Breast Cancer by Regulating Self-Renewal and Tumorigenesis of Stem Cells

The Mechanism and Function of Epigenetics in Uterine Leiomyoma Development

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