MicroRNA<i>miR-17-5p</i>is overexpressed in pancreatic cancer, associated with a poor prognosis, and involved in cancer cell proliferation and invasion

Yu, Jun; Ohuchida, Kenoki; Mizumoto, Kazuhiro; Fujita, Hayato; Nakata, Kenya; Tanaka, Masao

doi:10.4161/cbt.10.8.13083

Cited by 109 publications

(80 citation statements)

References 40 publications

(50 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, we hypothesized that the status of miR-17-92 cluster expression could be an independent factor for predicting the prognosis of this disease. These results were consistent with previous studies in pancreatic cancer and oesophageal squamous cell carcinomas [31,32].…”

Section: Discussionsupporting

confidence: 83%

Upregulation of microRNA-17-92 cluster associates with tumor progression and prognosis in osteosarcoma

Li¹,

Yang²,

Tian³

et al. 2014

neo

View full text Add to dashboard Cite

MicroRNA -17-92 (miR-17-92) cluster has been demonstrated to play a crucial role in various human cancers. However, its effects in osteosarcoma have not yet been elucidated. The purpose of this study was to investigate the clinical significance of miR-17-92 cluster in osteosarcoma. MiR-17-92 cluster expression in osteosarcoma clinical samples and cell lines was detected by real-time quantitative RT-PCR. Then, the association of miR-17-92 cluster level with survival of osteosarcoma patients was performed by the Kaplan-Meier and Cox proportional regression analyses. Furthermore, the effects of miR-17-92 cluster on tumorigenicity of osteosarcoma cell lines were evaluated by in vitro assays. The relative expression of miR-17-92 cluster in osteosarcoma tissues was significantly higher than those in adjacent normal tissues (P=0.001). And there was a relationship between miR-17-92 cluster upregulation and advanced TNM stage of osteosarcoma patients (P=0.037). Moreover, higher miR-17-92 cluster expression clearly predicted poorer Recurrence-free survival (P<0.001) and Overall survival (P=0.002). In the multivariate analysis, high miR-17-92 cluster expression was an independent prognostic factor for Recurrence-free survival (P<0.001) and Overall survival (P=0.002). Furthermore, the cellular proliferation, invasion, and migration of osteosarcoma cell lines were significantly accelerated by miR-17-92 cluster plasmid in vitro assays. Our findings showed that miR-17-92 cluster could serve as a promising marker for tumor recurrence and survival of osteosarcoma patients. Moreover, miR-17-92 cluster has been identified as a promoter for tumorigenicity of osteosarcoma cells, thus it might be a critical targeted therapy strategy for osteosarcoma.

show abstract

Section: Discussionsupporting

confidence: 83%

Upregulation of microRNA-17-92 cluster associates with tumor progression and prognosis in osteosarcoma

Li¹,

Yang²,

Tian³

et al. 2014

neo

View full text Add to dashboard Cite

show abstract

“…Expression profiling studies have revealed widespread overexpression of miR-17-5p in diverse tumor subtypes including both hematopoietic malignancies and solid tumors such as those derived from breast, colon and lung [15,16]. However, based on the previous studies it appears that miR-17-5p may have distinct effects in different kinds of tumors.…”

Section: Introductionmentioning

confidence: 94%

By Targeting Stat3 microRNA-17-5p Promotes Cardiomyocyte Apoptosis in Response to Ischemia Followed by Reperfusion

Du¹,

Pan²,

Chen³

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Several studies have confirmed the role of microRNAs in regulating ischemia/reperfusion-induced cardiac injury (I/R-I). MiR-17-5p has been regarded as an oncomiR in the development of cancer. However, its potential role in cardiomyocytes has not been exploited. The aim of this study is to investigate the role of miR-17-5p in I/R-I and the underlying mechanism through targeting Stat3, a key surviving factor in cardiomyocytes. Methods: MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide) assay was used to detect the cell viability. ELISA and TUNEL were performed to measure apoptosis of neonatal rat ventricular cardiomyocytes (NRVCs). Infarct area was estimated by TTC (triphenyltetrazolium chloride) and Evans blue staining. Western blot analysis was employed to detect the Stat3 and p-Stat3 levels and real-time RT-PCR was used to quantify miR-17-5p level. Results: The miR-17-5p level was significantly up-regulated in I/R-I mice and in NRVCs under oxidative stress. Overexpression of miR-17-5p aggravated cardiomyocyte injury with reduced cell viability and enhanced apoptotic cell death induced by H₂O₂, whereas inhibition of miR-17-5p by its antisense AMO-17-5p abrogated the deleterious changes. Moreover, the locked nucleic acid-modified antisense (LNA-anti-miR-17-5p) markedly decreased the infarct area and apoptosis induced by I/R-I in mice. Furthermore, overexpression of miR-17-5p diminished the p-Stat3 level in response to H₂O_2. The results from Western blot analysis and luciferase reporter gene assay confirmed Stat3 as a target gene for miR-17-5p. Conclusion: Upregulation of miR-17-5p promotes apoptosis induced by oxidative stress via targeting Stat3, accounting partially for I/R-I.

show abstract

“…Whereas there appears to be an oncogenic role for this miRNA in some cancers including melanoma (Segura et al 2009), endometrioid endometrial cancer (Myatt et al 2010), and glioma ; in others, such as lung adenocarcinoma (Sun et al 2010;Zhang et al 2011) and human gastric adenocarcinoma (Kong et al 2012), its role is more akin to that of a tumor suppressor. Such dual-function miRNAs have been previously reported: miR-26a (Sander et al 2008;Huse et al 2009;Kota et al 2009;Kim et al 2010), miR-205 (Iorio et al 2007, 2009Gandellini et al 2009;Wu et al 2009), and miR-17-5p (Hossain et al 2006;Mraz et al 2009;Yu et al 2010;Li et al 2011) are all characterized examples. In the latter case, the molecular mechanism underlying the dual phenotype was uncovered through systematic screening of predicted targets through luciferase assays (Cloonan et al 2008).…”

Section: Kip1mentioning

confidence: 99%

MicroRNA-182-5p targets a network of genes involved in DNA repair

Krishnan

Steptoe

Martin

et al. 2012

RNA

113

View full text Add to dashboard Cite

MicroRNAs are noncoding regulators of gene expression, which act by repressing protein translation and/or degrading mRNA. Many have been shown to drive tumorigenesis in cancer, but functional studies to understand their mode of action are typically limited to single-target genes. In this study, we use synthetic biotinylated miRNA to pull down endogenous targets of miR-182-5p. We identified more than 1000 genes as potential targets of miR-182-5p, most of which have a known function in pathways underlying tumor biology. Specifically, functional enrichment analysis identified components of both the DNA damage response pathway and cell cycle to be highly represented in this target cohort. Experimental validation confirmed that miR-182-5p-mediated disruption of the homologous recombination (HR) pathway is a consequence of its ability to target multiple components in that pathway. Although there is a strong enrichment for the cell cycle ontology, we do not see primary proliferative defects as a consequence of miR-182-5p overexpression. We highlight targets that could be responsible for miR-182-5p-mediated disruption of other biological processes attributed in the literature so far. Finally, we show that miR-182-5p is highly expressed in a panel of human breast cancer samples, highlighting its role as a potential oncomir in breast cancer.

show abstract

MicroRNAmiR-17-5pis overexpressed in pancreatic cancer, associated with a poor prognosis, and involved in cancer cell proliferation and invasion

Cited by 109 publications

References 40 publications

Upregulation of microRNA-17-92 cluster associates with tumor progression and prognosis in osteosarcoma

Upregulation of microRNA-17-92 cluster associates with tumor progression and prognosis in osteosarcoma

By Targeting Stat3 microRNA-17-5p Promotes Cardiomyocyte Apoptosis in Response to Ischemia Followed by Reperfusion

MicroRNA-182-5p targets a network of genes involved in DNA repair

Contact Info

Product

Resources

About