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5 publications mentioning hsa-mir-588

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-588. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 122
MiR-580, miR-588 and miR-190 also downregulated TIMP-3, an endogenous inhibitor of metalloproteinases, that was recently found to be involved in the dormancy process. [score:6]
We found that miR-588 expression and down-regulation of Bv8 preferentially impaired the recruitment of the Gr1+ myeloid cell population. [score:6]
Over -expression of DmiRs in A-GBM cells was confirmed by qRT-PCR (Information S1), and mice were injected with miR-580, miR-588, miR-190 or vector control (GFP) expressing A-GBM cells. [score:5]
Inhibition of tumor growth by expression of miR-580, miR-588 or miR-190 had also been observed in osteosaroma cell lines. [score:5]
Expression levels of genes in miR-580, miR-588 and miR-190 over -expressing A-GBM tumors were normalized to GFP-vector control. [score:5]
Percentage of Gr1 or CD11b expressing cells among CD45 positive cells in circulation of mice bearing fast-growing glioblastoma expressing either GFP (black bars) or miR-588 (dotted bars) was determined using FACS analysis. [score:5]
Proliferating tumor cells were also detected by Ki67 immunohistochemistry and representative photomicrographs are shown (D) in dormant miR-588 expressing GBMs (107days post implantation) and fast-growing GFP expressing control tumors (day 113 after implantation). [score:5]
Among the consensus miR-580, miR-588 and miR-190 upregulated transcripts, we found two important dormancy associated genes, i. e., EphA5 and Angiomotin. [score:4]
Hence, our data suggest that that miR-580, miR-588 and miR-190 downregulate Bv8 in a GCSF independent manner. [score:4]
These three DmiRs were selected based on their marked differential expression in dormant tumors; at least three out of four dormant tumors had an average of ∼ 12, 10 and 75-fold higher expression levels of miR-580, miR-588 and miR-190, as compared to the fast-growing tumors. [score:4]
To prove this hypothesis, we reconstituted the expression of miR-580, miR-588 or miR-190 in fast-growing A-GBM tumors. [score:3]
Size-matched GFP-vector-control and miR-588 expressing A-GBM tumors were harvested at day 35 post injection. [score:3]
The in-vivo apoptosis index for miR-588 expressing vs. [score:3]
Over -expression of miR-580, miR-588 and miR-190 in fast-growing angiogenic glioblastoma. [score:3]
In contrast, the tumor take rates were 80% (4/5) for miR-580, 75% (3/4) for miR-588 and only 40% (2/5) in miR-190 over -expressing tumors (Table 1). [score:3]
The expression level of miR-580, miR-588 and miR-190 was detected in human glioma specimens (C–E). [score:3]
Expression of miR-580, miR-588, miR-190 as well as the control-GFP-vector neither blocks cell proliferation nor enhances cell death even in-vitro at hyperconfluence state (after 144h) as determined by caspase 3/7 activity (Figure 2C). [score:3]
In line with our previous reports in these dormancy mo dels, the fraction of TUNEL positive apoptotic tumor cells was threefold increased in-vivo in dormant miR-588 expressing tumors vs. [score:3]
The reduced recruitment of Gr1+ myeloid cells also correlated with impaired angiogenesis in miR-588 expressing tumors as detected by CD31 staining of the tumor microvascular endothelium. [score:3]
Using qRT-PCR the efficacy of DmiR transfection was confirmed by analyzing their expression levels in miR-580, miR-588 or miR-190 vs. [score:3]
To test potential dormancy promoting functional effects of the identified DmiRs, lentiviral vectors encoding miR-580, miR-588 or miR-190 were used to reconstitute their expression in fast-growing angiogenic T98G human glioblastoma multiforme cells (A-GBM). [score:3]
A threefold increase in the fraction of TUNEL+ apoptotic tumor cells was found in dormant miR-588 expressing- vs. [score:3]
Unfortunately, the knowledge of the function and potential gene targets of miR-580, miR-588 and miR-190 is very limited and their contribution to cancer progression is unknown. [score:3]
Figure 2D shows the high rate of proliferative Ki67+ cells in a representative dormant miR-588 expressing A-GBM tumor at day 113 post injection. [score:3]
CD11b+ and Gr1+ myeloid cells were highly abundant in control A-GBM tumors, whereas their level was markedly reduced in miR-588 expressing tumors. [score:3]
Gr1+ myeloid cells were almost absent in miR-588 expressing tumors (Figure 5B). [score:3]
The in-vivo proliferation index for miR-588 expressing vs. [score:3]
This analysis revealed no significant difference in proliferation between the two groups (p = 0.12) with a trend toward more proliferation in dormant miR-588 expressing tumors. [score:3]
Average tumor volume of parental tumor (labeled in red line) n = 11, cells infected with GFP only control vector (n = 9), miR-580 (n = 5), miR-588 (n = 4), and miR-190 (n = 5) expressing A-GBM tumors. [score:3]
The median tumor free survival was markedly increased in miR-580 and miR-588 expressing tumors as compared to the GFP control. [score:2]
In line with the reduced recruitment of these cells detected in the tumor microenvironment, we found decreased levels of Gr1+/CD11b+ cells in circulation in miR-588 expressing tumors as compared to the levels in GFP-vector-control A-GBM (Figure 5C). [score:2]
To examine the regulation patterns of the identified DmiRs in primary human tumor tissue, the expression levels of miR-580, miR-588 and miR-190 in tissue specimens of glioma patients were investigated. [score:2]
The median “tumor free” period, i. e., the time until tumors were detected in 50% of the monitored animals in each group, was markedly prolonged in miR-588 (∼78 days) and miR-580 (∼103 days) expressing tumors as compared to GFP-vector-control (∼61 days) or non -transfected parental A-GBM (40 days) (Figure 2B). [score:2]
MiR-588-GFP or vector-control- GFP expressing A-GBM tumors were stained for Gr1/CD11b myeloid cell- or CD31 vascular endothelial marker. [score:2]
This analysis revealed no significant difference between the dormant miR-588 and the fast growing control (GFP) tumors (p = 0.12). [score:1]
control (GFP) A-GBM tumors was assessed by counting the fraction of Ki67+ tumor cells in 15 (miR-588) and 13 (control) representative high power fields (20x). [score:1]
Enhanced apoptosis was detected in-vivo in miR-588 vs. [score:1]
control (GFP) A-GBM tumors was assessed by counting the fraction of TUNEL+ tumor cells in 16 (miR-588) and 18 (control) representative high power fields (20x). [score:1]
For all subsequent confirmatory and functional validation studies, the top three dormancy -associated miRs miR-580, miR-588 and miR-190– were used. [score:1]
Impaired mobilization of Gr1 and CD11b positive myeloid cells in circulation of miR-588 tumor bearing mice (C). [score:1]
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[+] score: 23
The data shown in Table 1 and depicted in Fig 4 support the concept that treatment with anti-microRNA-210, but not with anti-microRNA-588, suppresses MTH -induced increases of the expression of these genes. [score:5]
The results demonstrate that microRNA-210 expression is inhibited following treatment with the anti-microRNA-210 of MTH -treated and untreated K562 cells, but not when anti-microRNA-588 was used (Fig 3B). [score:5]
Since our first interest was to identify sequences modulated by microRNA-210, we compared this list with a list of transcripts which were found to be both down-regulated in MTH -induced K562 cells (excluding the transcripts modulated in MTH -induced K562 cells plus anti-microRNA-588) and up regulated in MTH -induced K562 cells treated with anti-microRNA-210. [score:4]
As previously described, microRNA-210 is up regulated after MTH-treatment, while microRNA-588 is expressed at very low levels in K562 cells without major changes during MTH-treatment (data not shown) and was considered as an internal negative control of the experiment. [score:3]
The samples analyzed were obtained respectively from untreated K562 cells (a) or K562 cells treated with MTH (30 nM) + anti-microRNA-210 (b), MTH (c), or MTH + anti-microRNA-588 (d) (p<0.05). [score:1]
The samples analyzed were obtained from untreated K562 cells and K562 cells treated with MTH (30 nM) + anti-microRNA-210, MTH, or MTH + anti-microRNA-588 (taken as anti-microRNA-control). [score:1]
We found only minor changes after treatment of K562 cells with MTH plus anti-microRNA-588, while treatment with MTH plus anti-microRNA-210 displays a microarray profile that is more similar to control cells than MTH -induced cells (Fig 3A). [score:1]
To further investigate the role of microRNAs in MTH-treatment, the gene expression profiles of K562 cells treated with 30 nM MTH and MTH plus anti-microRNA-210 or anti-microRNA-588 were examined. [score:1]
0121567.g004 Fig 4 The samples analyzed were obtained respectively from untreated K562 cells (a) or K562 cells treated with MTH (30 nM) + anti-microRNA-210 (b), MTH (c), or MTH + anti-microRNA-588 (d) (p<0.05). [score:1]
In addition, administration of anti-microRNA-210 (but not of anti-microRNA-588) prevents MTH -mediated γ-globin mRNA accumulation (Fig 3C). [score:1]
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[+] score: 12
miR-588 but not miR-615-5p also suppressed hPGRN expression in stable cell lines (data not shown), indicating that multiple miRNAs may be potential targets for therapeutic manipulation of hPGRN levels. [score:7]
Two other miRNAs, miR-588 and miR-615-5p, were predicted to target hPGRN mRNA by more than two target prediction programs. [score:5]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-190a, hsa-mir-580, hsa-mir-190b
Recently, miR-34a was reported to negatively modulate chondrogenesis by targeting EphA5 in chick limb mesenchymal cells [61], whereas antiangiogenic and dormancy-promoting molecules including EphA5 were reported to be upregulated by expression of dormancy -associated miR-580, miR-588, and miR-190 [37]. [score:8]
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[+] score: 6
Although no miRNA has been proposed to directly target HIF-2 levels in human endothelium to date, recent work indicates that miR-588 in neuroblastoma stimulates HIF-2α expression through interaction with 5′ UTR of EPAS1 mRNA [139]. [score:6]
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