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4 publications mentioning hsa-mir-567

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-567. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 222
Other miRNAs from this paper: hsa-mir-188
Enhanced expression of FGF5 could partially antagonize the suppressive effects of miR-567 -overexpressing in OS cells. [score:7]
Furthermore, overexpression of miR-567 suppressed the FGF5 protein expression both in the MG-63 and U2OS cells (Figure 4C (Fig. 4)). [score:7]
In addition, the expression of miR-567 further confirmed in several common OS cell lines, including MG-63, U2OS and Saos-2. Consistently, miR-567 expression levels were significantly downregulated 0.84 ± 0.14 in MG-63 (p < 0.01), 0.68 ± 0.21 in U2OS (p < 0.01) and 0.45 ± 0.28 -fold in Saos-2 (p < 0.05) cell lines compared with normal human osteoblast cell line hFOB, respectively (Figure 1B (Fig. 1)). [score:7]
Moreover, we found ectopic expression of miR-567 increased the epithelial marker E-cadherin protein expression and decreased the mesenchymal marker Vimentin protein expression in both MG-63 and U2OS cells (Figure 3C (Fig. 3)). [score:7]
Moreover, overexpression of miR-567 was shown to increase E-cadherin expression and reduce Vimentin expression. [score:7]
miR-567 expression levels were downregulated in osteosarcoma tissues and cell lines. [score:6]
The expression of miR-567 was downregulated in OS tissues and cell lines. [score:6]
A previous study showed that miR-567 expression is aberrant in breast cancer, and ectopic expression of miR-567 impeded MDA-MB-231 cells proliferation and migration (Bertoli et al., 2017[2]). [score:5]
Here, heightened expression of miR-567 also displayed an inhibitory effect on the migration as well as invasion in OS cells. [score:5]
Our studies indicate that miR-567 functions as an inhibitor of EMT, which may at least partially though alteration of EMT biomarkers E-cadherin and Vimentin expression. [score:5]
Overexpression of FGF5 partially rescues the inhibitory effects of miR-567 in osteosarcoma cells. [score:5]
These findings further demonstrated that FGF5, as a target gene of miR-567, could antagonize the suppressive effects of miR-567 on OS cell proliferation and invasion. [score:5]
Enhanced expression of miR-567 inhibited the proliferative, migratory and invasive potential of OS cells. [score:5]
Moreover, overexpression of miR-567 decreased the Ki-67 and PCNA protein expression both in the MG-63 and U2OS cells (Figure 2C (Fig. 2)). [score:5]
In a previous study, overexpression of miR-567 has been implicated in the suppression of breast cancer cell migration. [score:5]
The putative targeting gene (FGF5) of miR-567 was predicted using TargetScan software (http://www. [score:5]
Elevated expression of miR-567 inhibited OS cell migration and invasion. [score:5]
For restoration of FGF5 expression, pcDNA3.1-FGF5 plasmid was used to transfect the miR-567 -overexpressing MG-63 and U2OS cells, while control vector was used as control. [score:5]
As shown in Figure 1A (Fig. 1), miR-567 expression levels in OS tissues were significantly downregulated compared to those in the adjacent non-tumor tissues (p < 0.001). [score:5]
Elevated expression of miR-567 suppressed the osteosarcoma cell migration and invasion ability. [score:5]
Elevated expression of miR-567 suppressed the OS cell proliferation. [score:5]
Elevated expression of miR-567 suppressed the osteosarcoma cell proliferation. [score:5]
Enhanced expression of miR-567 have low proliferative, migratory and invasive capabilities though interfere translational levels of FGF5. [score:5]
As a result, miR-567 was significantly downregulated in OS tissues and cell lines by using RT-PCR. [score:4]
In particular, FGF5 is a putative target of miR-567 as predicated by TargetScan and luciferase reporter assay. [score:4]
Simultaneous overexpression of miR-567 appears to have a negative effect in regulating FGF5, then resulted in a significant change in proliferation and EMT biomarkers. [score:4]
CCK-8 assay indicated that ectopic expression of miR-567 suppressed the MG-63 (p < 0.001) and U2OS (p < 0.01, p < 0.001) cell proliferation (Figure 2B (Fig. 2)). [score:4]
FGF5 was a direct target gene of miR-567. [score:4]
Similarly, upregulation of miR-567 remarkably decreased the number of invasive cells in U2Os cells. [score:4]
FGF5 was a direct target gene of miR-567 in osteosarcoma cells. [score:4]
The results of Transwell experiments indicated that upregulation of miR-567 could restrict the migratory and invasive ability of MG-63 and U2OS cells (Figure 3A and B (Fig. 3), p < 0.001). [score:4]
Our study provides the basis for using miR-567 as a novel therapeutic target in OS. [score:3]
As FGF5 has been reported to be involved in multiple tumor cell proliferation and metastasis (Fang et al., 2015[7]; Hanada et al., 2001[10]), it was thus speculated that FGF5 might mediate the inhibitory effect of miR-567 on cell proliferation, migration and invasion in OS. [score:3]
In summary, our study indicated that miR-567 expression levels were reduced in OS tissues and cell lines. [score:3]
The relative expression of miR-567 was determined for tissue samples and cell lines using 2 [-ΔΔCT] method (Livak and Schmittgen, 2012[17]). [score:3]
However, the function of miR-567 in regulating OS development and progression are still unknown. [score:3]
For miR-567 overexpression, miR-567 mimics were transfected into MG-63 and U2OS cells, while oligonucleotide scramble were used as a negative control. [score:3]
Furthermore, FGF5 was predicted and demonstrated as the potential target gene of miR-567. [score:3]
We first performed qRT-PCR to determine the expression of miR-567 in a total of 20 OS tissues and matched adjacent non-tumor tissues. [score:3]
In the current study, we attempt to determine the expression and biological function of miR-567 in the OS. [score:3]
In the present study, we first show that miR-567 is poorly expressed in OS tissues and OS cell lines. [score:3]
Here, enhanced expression of miR-567 exhibited a significant anti-proliferative effect in OS cells, MG-63 and U2OS. [score:3]
To verify this hypothesis, we performed rescue experiments by transfecting pcDNA3.1-FGF5 plasmid into miR-567 -overexpressing OS cells and examined cell function. [score:3]
In this study, overexpression of FGF5 partially restores the impaired cell proliferation, migration and invasion induced by miR-567, supporting a key role of FGF5 signaling in these pathological processes. [score:3]
org), FGF5 could be one of the target genes of miR-567 (Figure 4A (Fig. 4)). [score:3]
As shown in Figure 4B (Fig. 4), the luciferase reporter assay showed that only MG-63 and U2OS cells in the WT 3'UTR + miR-567 mimics group had a remarkably lower luciferase activity than other groups (p < 0.001), suggesting that miR-567 could restrain FGF5 translation by binding to its 3'UTR. [score:2]
CCK-8 assay indicated that overexpression of FGF5 partially rescued the impaired cell proliferation induced by miR-567 mimics in MG-63 and U2OS cells (Figure 5B (Fig. 5), p < 0.01, p < 0.001). [score:2]
Additionally, showed that miR-567 negatively regulated two cell proliferative markers Ki-67 and PCNA. [score:2]
To investigate the function of miR-567 on OS development, MG-63 and U2OS with lower miR-567 expression were selected for transfection with miR-567 mimics or scramble plasmid. [score:2]
As shown in Figure 2A (Fig. 2), transfection with miR-567 mimics led to a significant increase in miR-567 expression levels compared with those in scramble control group, confirmed by qRT-PCR in both MG-63 and U2OS cells (p < 0.001). [score:2]
In addition, a high frequency of miR-567 mutation was found in colorectal cancer cells and primary tumors (El-Murr et al., 2012[6]). [score:2]
Notably, our results revealed miR-567 as endogenous modulator of FGF5 and confirmed the importance of miR-567-FGF5 interaction for the proliferation, migration and invasion in OS cell lines. [score:1]
As for cell invasion, the number of invasive cells was reduced from 116.7 ± 4.2 in miR-567 mimics group to 55.3 ± 10.8 in scramble group in MG-63. [score:1]
Disturbance of EMT played a major role in the attenuation of miR-567 -induced OS cell migration and invasion. [score:1]
After transfection, the protein level of FGF5 was significantly higher in the FGF5 + miR-567 group than that in the control + miR-567 group (Figure 5A (Fig. 5)). [score:1]
Because miR-567 responsive genes Ki-67 and PCNA are known cell-cycle genes, one predication is that OS cells with miR-567 deficiency will promote cell proliferation by activating the cell cycle progression and DNA replication. [score:1]
The average number of migratory cells in the miR-567 mimics group was significantly less than that in the scramble group (MG-63: 22.3 ± 1.5 vs. [score:1]
These data suggest miR-567 might play the key roles in the tumor progression of OS. [score:1]
MG-63 and U2OS cells were transfected with miR-567 mimics or co -transfected with miR-567 mimics and FGF5 plasmid. [score:1]
Shao et al. (2017[25]) pointed out that miR-567 can be used for a predictive marker in non-small-cell lung cancer diagnosis. [score:1]
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2
[+] score: 20
Expression of miR-567 and miR-1273c was not detectable in colonic mucosae and colorectal cell lines (C [T]>36 cycles) (data not shown); whereas miR-1303 appeared to be fairly expressed in both normal and tumor colonic cells (Figure 5B). [score:5]
Note that hsa-mir-644 is included in the group of miRNAs rarely or not mutated in MSI CRCs (n = 18, frequency of mutation <25%) whereas hsa-mir-1273c, hsa-mir-567 and hsa-mir-1303 constitute the group of miRNAs frequently altered (n = 3, frequency of mutation >75%). [score:3]
Our analysis allowed the identification of 3 MSI -targeted miRNAs: hsa-mir-1273c, hsa-mir-567 and hsa-mir-1303. [score:3]
Note that hsa-mir-644 is incorporated in the group of miRNAs frequently altered, that also includes hsa-mir-1273c, hsa-mir-567 and hsa-mir-1303 (n = 4, frequency of mutation >45%). [score:2]
A bi-allelic mutation was also noted in 36%, 57% and 83% of altered MSI CRC cell lines for mir-1273c, mir-567 or mir-1303, respectively (Figure 4, Table S2). [score:2]
0031862.g004 Figure 4MNR instabilities in hsa-mir-1273c (T11), hsa-mir-567 (A13) and hsa-mir-1303 (T13). [score:1]
The second group contained 3 miRNA genes (hsa-mir-1273c, hsa-mir-567 and hsa-mir-1303) frequently mutated in MSI CRCs (≥75%). [score:1]
For the detection of miR-567, the miScript PCR system (miScript RT and miScript SYBR Green PCR kits) was used according to the manufacturer's instructions (Qiagen). [score:1]
By screening the quasi totality of MNR and DNR (≥7 repeat units) contained in miRbase-V15-annotated miRNA hairpin sequences, hsa-mir-1273c, hsa-mir-1303 and hsa-mir-567 were demonstrated to be mutated at high frequency in both CRC cell lines and primary tumors. [score:1]
MNR instabilities in hsa-mir-1273c (T11), hsa-mir-567 (A13) and hsa-mir-1303 (T13). [score:1]
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3
[+] score: 5
Other miRNAs from this paper: hsa-mir-299, hsa-mir-609, hsa-mir-297, oar-mir-299
miRNA, such as miRNA-297, miRNA-299, miRNA-567 and miRNA-609 are able to control its expression by preventing protein production without inhibition of the transcription [28]. [score:5]
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4
[+] score: 3
On the one hand, the CARE is targeted by at least four different miRNAs (miR-297, miR-299, miR-567, and miR-609) and by the heterogeneous nuclear ribonucleoprotein L (hnRNP L). [score:3]
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