miRNA profiling in metastatic renal cell carcinoma reveals a tumour-suppressor effect for miR-215

White, Nicole M.; Khella, Heba; Grigull, Jörg; Adzovic, Sonja; Youssef, Yousef M.; Honey, R. John D'a.; Stewart, Robert; Pace, Kenneth T.; Bjarnason, Georg A.; Jewett, Michael A.S.; Evans, Andrew; Gabril, Manal; Yousef, George M.

doi:10.1038/bjc.2011.401

Cited by 152 publications

(112 citation statements)

References 44 publications

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“…Finally, we provide the first demonstration that ANKHD1 mRNA and protein are significantly enhanced in human ccRCC when compared to control, and may play an important role, in human ccRCC. (6,(26)(27)(28)(29)(30)(31), a finding that correlates with the upregulation of ANKHD1, demonstrated here. Furthermore, given that single inhibition of miRNA-29a is sufficient to restore the proliferation of RCC cells lacking ANKHD1, we suggest that miR-29a-targeted genes are likely to be responsible for the ANKHD1-mediated proliferation of ccRCCs.…”

Section: Discussionsupporting

confidence: 53%

Ankyrin repeat and single KH domain 1 (ANKHD1) drives renal cancer cell proliferation via binding to and altering a subset of miRNAs

Fragiadaki

Zeidler

2018

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 53%

Ankyrin repeat and single KH domain 1 (ANKHD1) drives renal cancer cell proliferation via binding to and altering a subset of miRNAs

Fragiadaki

Zeidler

2018

Journal of Biological Chemistry

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“…miR-215 is upregulated in cervical cancer , hepatocellular carcinoma , gastric cancer (Deng et al, 2014), and prostate cancer (Walter et al, 2013), and it acts as a potential oncogene in these tumors. On the contrary, the expression of miR-215 was found to be significantly decreased in esophageal adenocarcinoma (Wijnhoven et al, 2010), colon cancer (Karaayvaz et al, 2011), and renal cell carcinoma (RCC) (White et al, 2011), where it acts as a candidate tumor suppressor. However, the correlation between miR-215 dysregulation and clinicopathological characteristics of pancreatic cancer has not yet been evaluated, and the biological roles of miR-215 and its direct functional targets in pancreatic cancer remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer

Qw¹,

Zhou²,

F³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. It has been shown that microRNA-215 (miR-215) is dysregulated in several human malignancies, and this correlates with tumor progression. However, its expression and function in pancreatic cancer is still unclear. The aim of this study was to explore the effects of miR-215 on pancreatic cancer formation and progression. Using quantitative RT-PCR, we detected miR-215 expression in pancreatic cancer cell lines and primary tumor tissues. The association of miR-215 expression with clinicopathological factors and prognosis was also analyzed. We then observed the effects of miR-215 on the biological behavior of pancreatic cancer cells. Lastly, the potential regulatory function of miR-215 on ZEB2 expression was investigated. miR-215 expression levels were significantly downregulated in pancreatic cancer samples and cell lines. Decreased miR-215 expression was significantly associated with large tumor size, advanced TNM stage, lymph node metastasis, vessel invasion, and lower overall survival. Multivariate regression analysis corroborated that downregulation of miR-215 was an independent unfavorable prognostic factor. Overexpression of miR-215 inhibited pancreatic cancer cell 16133-16145 (2015) proliferation, invasion, and migration; promoted cell apoptosis in vitro; and suppressed tumorigenicity in vivo. Further, ZEB2 was confirmed as a direct target of miR-215 by using a luciferase reporter assay. These findings indicate that miR-215 may act as a tumor suppressor in pancreatic cancer cells, and could serve as a novel therapeutic target for miR-based therapy.

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“…The miRNA-target prediction revealed that these three genes were direct targets of these miRNAs. Low expression of miR128, but not miR502-5p or miR-215/625 [14], significantly correlated with poor patient OS in both the training set and the validation sets, which is consistent with other reports for breast and colon cancers [15,16]. Moreover, patients with higher expression of CCND1 and lower expression of miR-502-5p had significantly poorer OS than did patients with lower CCND1 expression and higher miR502-5p expression.…”

Section: Discussionsupporting

confidence: 81%

Comprehensive epigenetic analysis of Notch pathway in high-grade serous ovarian cancer

Ivan

Bottsford-Miller

et al. 2013

Gynecologic Oncology

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Objectives-Gene methylation and other epigenetic modifications of gene regulation have been implicated in the growth of ovarian cancer, but the clinical significance of such modifications in the Notch pathway in high-grade serous ovarian cancer (HGS-OvCa) is not well understood. We used The Cancer Genome Atlas (TCGA) data to study the clinical relevance of epigenetic modifications of Notch pathway genes.Methods-We analyzed the interaction of DNA methylation and miRNAs with gene expression data for Notch family members with the Spearman rank correlation test and explored potential relationships with overall survival (OS) with the log-rank test. We downloaded clinical data, level 3 gene expression data, and level 3 DNA methylation data for 480 patients with stage II-IV HGSOvCa from TCGA data portal. Patients were randomly divided into training and validation cohorts for survival analyses. In each set, patients were grouped into percentiles according to methylation and microRNA (miRNA) or messenger RNA (mRNA) levels. We used several algorithms to predict miRNA-mRNA interaction. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.No conflicts of interest were disclosed. Conflict of interest statementThe authors declare that there are no conflicts of interest. Results-There were significant inverse relationships between methylation status and mRNA expression for PPARG, CCND1, and RUNX1. For each of these genes, patients with a lower methylation level and higher expression level had significantly poorer OS than did patients with a higher methylation level and lower expression level. We also found a significant inverse relationship between miRNAs and mRNA expression for CCND1, PPARG, and RUNX1. By further analyzing the effect of miRNAs on gene expression and OS, we found that patients with higher levels of CCND1, PPARG, and RUNX1 expression and lower expression levels of their respective miRNAs (502-5p, 128, and 215/625) had significantly poorer OS. NIH Public AccessConclusions-Epigenetic alterations of multiple Notch target genes and pathway interacting genes (PPARG, CCND1, and RUNX1) may relate to activation of this pathway and poor survival of patients with HGS-OvCa.

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miRNA profiling in metastatic renal cell carcinoma reveals a tumour-suppressor effect for miR-215

Cited by 152 publications

References 44 publications

Ankyrin repeat and single KH domain 1 (ANKHD1) drives renal cancer cell proliferation via binding to and altering a subset of miRNAs

Ankyrin repeat and single KH domain 1 (ANKHD1) drives renal cancer cell proliferation via binding to and altering a subset of miRNAs

MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer

Comprehensive epigenetic analysis of Notch pathway in high-grade serous ovarian cancer

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