MicroRNA signatures in human ovarian cancer.

By Marilena V. Iorio, R. Visone, Gianpiero di Leva, V. Donati, F. Petrocca, P. Casalini, Cristian Taccioli, Stefano Volinia, Chang-Gong Liu, H. Alder and 3 more. Cancer Research, 2007

1,280 citations recorded by the source corpus.

Epithelial ovarian cancer (EOC) is the sixth most common cancer in women worldwide and, despite advances in detection and therapies, it still represents the most lethal gynecologic malignancy in the industrialized countries. Unfortunately, still relatively little is known about the molecular events that lead to the development of this highly aggressive disease. The relatively recent discovery of microRNAs (miRNA), a class of small noncoding RNAs targeting multiple mRNAs and triggering translation repression and/or RNA degradation, has revealed the existence of a new level of gene expression regulation. Multiple studies involving various types of human cancers proved that miRNAs have a causal role in tumorigenesis. Here we show that, in comparison to normal ovary, miRNAs are aberrantly expressed in human ovarian cancer. The overall miRNA expression could clearly separate normal versus cancer tissues. The most significantly overexpressed miRNAs were miR-200a, miR-141, miR-200c, and miR-200b, whereas miR-199a, miR-140, miR-145, and miR-125b1 were among the most down-modulated miRNAs. We could also identify miRNAs whose expression was correlated with specific ovarian cancer biopathologic features, such as histotype, lymphovascular and organ invasion, and involvement of ovarian surface. Moreover, the levels of miR-21, miR-203, and miR-205, up-modulated in ovarian carcinomas compared with normal tissues, were significantly increased after 5-aza-2'-deoxycytidine demethylating treatment of OVCAR3 cells, suggesting that the DNA hypomethylation could be the mechanism responsible for their overexpression. Our results indicate that miRNAs might play a role in the pathogenesis of human EOC and identify altered miRNA gene methylation as a possible epigenetic mechanism involved in their aberrant expression.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c0eb28d12221396ec223fbcc61168e54adf26e4c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

microRNA as Biomarkers and Diagnostics (2016, background): “…studies have shown altered miRNA profiles in multiple cancer types, such as breast cancer (Iorio et al., 2005), leukemia (Calin et al., 2004a), liver cancer (Qi et al., 2013), ovarian cancer (Iorio et al., 2007), pancreatic cancer (Wang and Sen, 2011), and prostate cancer (Porkka et al., 2007).”
miRNAs as Biomarkers in Disease: Latest Findings Regarding Their Role in Diagnosis and Prognosis (2020, background): “Other upregulated miRNAs in ovarian cancer tissues are miR-199a, miR-200a, miR-200b, miR-200 [132] and miR-200c, the latter being highly expressed only in the serous epithelial type [133].”
Normalization of microRNA expression levels in quantitative RT-PCR assays: identification of suitable reference RNA targets in normal and cancerous human solid tissues. (2008, background): “To date, only a handful of miRNA qRT-PCR studies have described some form of normalization, using RNA targets such as 5S (Takamizawa et al. 2004; Pineles et al. 2007), U6 (Choong et al. 2007; Corney et al. 2007; Shell et al. 2007), 18S (Iorio et al. 2007), or miR-16 or let-7a (Mattie et al. 2006).”
MicroRNAs in cancer: small molecules with a huge impact. (2009, background): “Interestingly, the results obtained by this genomic analysis were largely overlapping with the expression profiles on the same tumor types.(18,50)”
Reprogramming of miRNA networks in cancer and leukemia. (2010, neutral): “, E-TABM-664 (Bloomston et al. 2007), E-TABM-762 and E-TABM-763 (Visone et al. 2009), E-TABM-508 (Pichiorri et al. 2008) , E-TABM-429 (Garzon et al. 2008a), E-TABM-434 (Petrocca et al. 2008), E-TABM-405 (Garzon et al. 2008b), E-TABM-343 (Iorio et al. 2007), E-TABM-41 and E-TABM-42 (Calin et al. 2005”
MicroRNA and cancer (2012, background): “On the other hand, potentially oncogenic miRNAs can be upregulated by DNA hypomethylation (Brueckner et al., 2007; Iorio et al., 2007).”
PolymiRTS Database 3.0: linking polymorphisms in microRNAs and their target sites with human diseases and biological pathways (2013, neutral): “microarray) (21) and low-throughput (e.”
The detection of differentially expressed microRNAs from the serum of ovarian cancer patients using a novel real-time PCR platform. (2009, background): “While miRNA research in gynecologic malignancies is in its infancy, the miRNA signature profile of ovarian cancer has recently been published [12] [13] [14].”
The mammalian ovary from genesis to revelation. (2009, background): “Interestingly,mir-199alevelswerelowerinovarian cancers compared with normal ovary (645), but higher in ovarian cancers compared with an IOSE cell line (649).”
miR-21: a small multi-faceted RNA (2008, background): “[3, 53, 58, 60] Ovarian cancer Up-regulation [6, 7] Colorectal cancer Up-regulation Cellular outgrowth, migration, invasion and metastasis PDCD4, NFIB, SPRY2 [3, 25, 52, 86] Stomach/gastric cancer Up-regulation RECK [3, 5] Hepatocellular carcinoma Up-regulation Cell migration and invasion and…”
Modulation of K-ras-dependent lung tumorigenesis by microRNA-21 (2010, positive): “…lines showed increased miR-21 expression in glioblastoma (Chan et al., 2005; Ciafre et al., 2005), head and neck carcinomas (Tran et al., 2007), ovarian cancer (Iorio et al., 2007), B cell lymphoma (Lawrie et al., 2007), hepatocellular (Meng et al., 2007), and cervical carcinoma (Lui et al., 2007).”