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5 publications mentioning hsa-mir-562

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-562. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 214
The same notions apply to attempting to down-regulate expression of miR26b* or miR562 in order to down-regulate NF-κB activity in breast cancer cells. [score:9]
However, transfection of ANXA1 with miR562 results in a significant inhibition in TNFα expression when compared to miR562 transfection alone, indicating that ANXA1 may inhibit the TNFα expression induced by miR562, which may regulate angiogenic activity. [score:9]
qPCR analysis demonstrated that 7/11 NF-κB -dependent genes were downregulated to less than 0.5-fold after transfecting with miR26b*, and 6/11 NF-κB -dependent genes were downregulated to less than 0.5-fold after transfecting with miR562, confirming the inhibition of NF-κB activity. [score:9]
A decrease in fold-induction of NF-κB-promoter activity after PMA treatment was observed in cells over -expressing either miR26b* or miR562, indicating that miR26b* and miR562 was able to down-regulate NF-κB activity (Fig. 3C), while miRs were overexpressed (Fig. 3D). [score:8]
This data confirm that miR26b* and miR562 directly target and down-regulate RNA and protein levels of Rel A/p65 and NF-κB1/p105, respectively. [score:7]
0114507.g003 Figure 3 (A,B) qPCR expression of NFKB1 after miR26b* and miR562 overexpression in MCF7 and MCF7-V5 cells (overexpressing ANXA1). [score:7]
Functionally, higher expression of both miR26b* and miR562 in MCF7 cells lead to increased endothelial cell tube formation while inhibition of miR26b* and miR562 inhibited tube formation. [score:7]
In summary, we have shown that ANXA1 can modulate the expression of miR26b* and miR562, which are able to functionally down-regulate NF-κB activity both at promoter and downstream effector levels, which may lead to higher endothelial cell tube formation and lower wound healing capacity (with respect to miR562). [score:6]
This indicates again that ANXA1 down-regulates miR562, which may be involved in inhibition of wound healing in MCF7 breast cancer cells. [score:6]
The elucidation of molecular targets of miR26b* and miR562 has shed more light on miR regulation on NF-κB subunit expression. [score:6]
Our studies have contributed to understanding the ANXA1-NF-κB signaling paradigm further, highlighted the regulation 2 miRNAs by ANXA1, namely miR26b* and miR562 which directly targeted an NF-κB subunit REL-A (p65) and NF-κB1 (p105), respectively. [score:5]
NF-κB activity was inhibited by both miR26b* and miR562, leading to the inhibition of NF-κB dependent genes which are important in wound healing/migration and angiogenesis. [score:5]
NF-κB1 was inhibited after transfecting MCF-7 cells with miR26b* or miR562, and this inhibition was reversed in MCF7-V5 ANXA1 stably transfected cells (Fig. 3A,B). [score:5]
miR26b* and miR562 overexpression in MCF7 cells enhances endothelial cell angiogenesis while silencing miR26b* and miR562 inhibits angiogenesis. [score:5]
Interestingly, transfection of miR562 into ANXA1 overexpressing MCF7 cells reversed this inhibition in migration (Fig. 5C,D). [score:5]
miR562 overexpression in MCF7 cells inhibits wound healing. [score:5]
Direct targeting of Rel A and NF-κB1 by miR26b* and miR562 respectively contributes to the understanding of how NF-κB subunits can be regulated post-transcriptionally. [score:5]
It can be postulated that high expression of ANXA1 leads to a lower expression of miR26b* and miR562 which results in increased NF-κB activity. [score:5]
This data suggest that miR26b* and miR562 expressed in breast cancer cells can regulate tube formation by endothelial cells. [score:4]
We next determined if NF-κB -dependent genes such as MMP1 or MMP9 were also downregulated in MCF-7 cells transfected with miR26b* or miR562 (Fig. 3D,E). [score:4]
Lower levels of miR-26b* (Fig. 2E) and miR562 (Fig. 2F) were expressed in MDA-MB231 with no significant change in MCF-7. These data confirm that high levels of ANXA1 correlate with low levels of miR-26b* and miR562. [score:3]
However, a significant inhibition of wound closure was observed after miR562 transfection, 6 h and 24 h after the wound was made (Fig. 5A,B). [score:3]
3′UTR cloning and target analysis of miR26b*/RelA and miR562/NF-κB1. [score:3]
Hence, the ANXA1-NF-κB signaling paradigm described previously by Bist et al [7] has gained clarity with miR26b* and miR562 being able to target p65 and p105 respectively. [score:3]
These observations demonstrate that has-miR26b* and has-miR562 target Rel A and NF-κB1 at the 3′ UTR respectively. [score:3]
In MCF7 cells where either miR26b* or has-miR562 was inhibited, there was a reduction in the average number of tubes formed (Fig. 6C). [score:3]
MicroCOSM, a bioinformatics prediction tool, was used to predict putative targets of miR26b* and miR562 which were related to the NF-κB pathway. [score:3]
To confirm that NF-κB was indeed modulated by the 2 miRs studied, HEK 293T cells transiently expressing either miR26b* or miR562 were transfected with a construct harboring a NF-κB -binding site upstream of a luciferase reporter and stimulated with PMA. [score:3]
Anti-miR26b* and anti-miR562 might prove to be effective angiostatic agents to inhibit tumor angiogenesis, thus curbing further growth and metastasis. [score:3]
Fig. 2A–C show that miR26b* and miR562 expression are reduced when ANXA1 is high. [score:3]
Both miR26b* and miR562 over -expression in MCF7 cells resulted in an increase in average number of tubes formed (Fig. 6A,C) as well as average length of tubes formed (Fig. 6B,D). [score:3]
miR26b* and miR562 overexpression modulates NF-κB activity. [score:3]
As we have previously shown that ANXA1 can regulate NF-κB activity [7], we next elucidated if miR26b* or miR562 could be regulating NF-κB. [score:3]
p105 protein levels was  =  reduced when miR562 was transfected into MCF-7 cells, with an increase when ANXA1 was overexpressed. [score:3]
miR26b* and miR562 targets REL-A and NFκB1, respectively. [score:3]
Conversely, we also show that higher expression of miR26b* and miR562 can result in reduced NF-κB activity. [score:3]
Similarly, RNA levels of NF-κB1 were reduced in MCF7 cells transiently over -expressing miR562 (Fig. 4E). [score:3]
Interestingly, transfection of MCF-7 cells with ANXA1 overexpression plasmid did not affect tube formation, yet cotransfection of ANXA1 with miR562 reversed the increased tube length induced with mir562 alone (Fig. 7B). [score:3]
With respect to miR562, NF-κB1 and NF-κB activating protein were two NF-κB related genes predicted as targets. [score:3]
Expression of miR26b* and miR562 in breast cancer cells. [score:3]
S1 Fig MiR26b* and miR562 overexpression in MCF7 cells does not modulate proliferation. [score:3]
MiR562 overexpression in MCF7 cells induces secreted factors which enhance angiogenic activity of endothelial cells. [score:2]
Next, the endothelial cell tube formation assay was performed to assess the effect of miR26b* and miR562 expression in MCF7 cells on endothelial cell tube formation (co-culture). [score:2]
miR26b* and miR562 regulate NFκB activity in breast cancer cells. [score:2]
To determine if miR562 could be regulating the secretion of factors from MCF7 cells which could influence endothelial cell tube formation, MCF7 conditioned media was collected from control and miR562 -transfected cells and used to treat HUVEC for 24 h. Once again, treatment of HUVEC with conditioned media obtained from miR562 -transfected cells significantly enhanced the number of HUVEC tubes formed as well as the length of the tubes (Fig. 7A,B), with representative images shown in Fig. 6C. [score:2]
miR26b* and miR562 have been shown to regulate endothelial cell tube formation in MCF7 cells, which relates to angiogenesis. [score:2]
Only TNFα was significantly increased in MCF-7 cells transfected with miR562 (Fig. 7D), with no effect on anti-angiogenesis genes (Fig. 7E). [score:1]
The seed sequences of both has-miR26b* and has-miR562 have 6 nucleotides, out of which 5 are binding nucleotides (Fig. 4A,B). [score:1]
miR26b* is located on chromosome 2 at co-ordinates 219267369–219267455 and miR562 is located on the same chromosome 2 at co-ordinates 233037363–233037457 (Fig. 1C). [score:1]
0114507.g002 Figure 2 (A–C) RNA from MCF10A breast epithelial cells, MCF7 and MDA-MB231 breast cancer cells were isolated and expression levels of ANXA1, miR26b* and miR562 were measured. [score:1]
0114507.g007 Figure 7 (A,B) MCF7 cells were transfected with empty vector (EV), miR562, ANXA1 or cotransfected with ANXA1 and miR 562 and conditioned media was used to culture HUVEC in matrigel. [score:1]
More significantly, two novel miRs, hsa-miR26b* and hsa-miR562 were characterized and their targets were elucidated and experimentally validated. [score:1]
0114507.g006 Figure 6 MCF7 cells were transfected with empty vector (EV), miR26b* or miR562 and a co-culture using transwells was performed with HUVEC in matrigel. [score:1]
0114507.g005 Figure 5(A) MCF7 cells were transfected with empty vector (EV), miR26b* or miR562 and wound healing was observed at 0 h, 6 h and 24 h. Representative pictures are presented and (B) % wound closure analyzed. [score:1]
To confirm this, cell cycle analysis was performed and once again, no difference in cell cycle progression was observed for both miRNAs, indicating that both miR26* and miR562 do not affect proliferation in MCF7 cells. [score:1]
MCF7 cells were transfected with empty vector (EV), miR26b* or miR562 and (A) proliferation rates analyzed using crystal violet staining daily (B) or cell cycle analysis performed using propidium iodide staining. [score:1]
Similar co-culture experiments were performed with MCF7 cells silenced with control, anti-miR26b* and anti-miR562. [score:1]
MCF7 cells were transfected with empty vector (EV), miR26b* or miR562 and a co-culture using transwells was performed with HUVEC in matrigel. [score:1]
Subsequently, the precursor forms of hsa-miR26b*(miR26b*) and hsa-miR562 (miR562) were selected and cloned from human blood peripheral monocytes. [score:1]
Effects of miR26b* and miR562 on wound healing. [score:1]
miR26b* and miR562 enhance tumor cell induced endothelial cell tube formation. [score:1]
To assess which possible factors could be produced by miR562 -transfected MCF-7 cells, we performed real time PCR for pro-angiogenesis such as VEGF and TNFα, and anti-angiogenesis genes such as angiopoeitin-2 (ANG2) and thrombospondin (THBS1). [score:1]
S1 Fig. illustrates that no difference in growth rates were observed when either miR26b* or miR562 were transfected under the conditions studied (S1 Fig. ). [score:1]
The same observation was recorded in 3′ UTR analysis of NF-κB1 when miR562 was transfected into HEK 293T cells (56.7±10.7% rescue, Fig. 4E). [score:1]
We have shown that endogenous levels of miR26b* and miR562 are lower in MDA-MB-231 cells where ANXA1 levels are high and NF-κB activity is constitutively active. [score:1]
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[+] score: 7
Similarly, miR-562 contains an in del, the 18 bp deletion rs140596642, removing a large portion of the miRNA including the seed region, which may play a critical role in the development of Wilms’ tumor by both causing increased expression of miR-562 and dysregulation of its targets including EYA1 [53]. [score:7]
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[+] score: 5
let-7g-5p, miR-142-3p, miR-16-5p and miR-223-3p were expressed at high levels in all 5 lineages, while miR-134, miR-517c-3p/519a-3p, miR-518d-3p, miR-520d-5p/518a-5p/527 and miR-562 were expressed at low levels in all 5 lineages (Table S5B). [score:5]
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[+] score: 5
Among the differentially expressed miRNAs, 11 (miR-199a-5p, miR-218, miR-409a, miR-433, miR-511, miR-514, miR-551, miR-562, miR-556-3p, miR-1178 and miR-1205) were common to both doses (Figure 2D) and exhibited similar expression patterns (Tables 1A and C). [score:5]
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[+] score: 1
MNPT) miR-449a# 3.92 miR-32 3.49 miR-548c-5p 2.71 miR-562 2.56 miR-103-as 2.53 miR-512-3p 2.41 miR-200c* 2.33 miR-147b 2.24 miR-770-5p 2.09 miR-518c* 2.00 miR-517b 1.88 miR-182 1.79 miR-615-3p 1.70 miR-496 1.59 miR-1200 1.58 miR-375 1.54 miR-551a 1.53 *Passanger strand. [score:1]
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