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1 publications mentioning hsa-mir-3908

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-3908. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 253
Other miRNAs from this paper: hsa-mir-221
These outcomes verified that the mRNA of AdipoR1 is the direct target of miR-3908, and suppresses protein expression of its downstream pathway genes, including AMPK, p-AMPK, and SIRT-1. Therefore, this provides a new therapy target for BC treatment. [score:10]
Moreover, miR-3908 could enhance its migration, but the phenomenon was reversed by inhibitors of miR-3908 as well as by Flotillin-1. miR-3908 suppressed the interaction between AdipoR1 and Flotillin-1 by inhibiting the expression of the AdipoR1 or AMPK/SIRT1 signaling pathway. [score:9]
Our work firstly demonstrated that AdipoR1 is one of the targets of miR-3908 which regulates the expression of AdipoR1 followed by regulation of the AMPK/SIRT-1 signaling pathway. [score:7]
Altogether, our results demonstrated that miR-3908 directly regulates the expression of AdipoR1 by interacting with its 3’-UTR, and then the protein expression of its downstream genes. [score:7]
miR-3908 inhibited the mRNA expression of AdipoR1 in MCF-7 cells (a), as well as the protein expression of AdipoR1 (b). [score:7]
Following overexpression of miR-3908 in MCF-7 cells compared to NC, Western blot analyses verified that protein expression levels of AdipoR1 downregulated in MCF-7 cells induced by miR-3908. [score:7]
Furthermore, the inhibitors of miR-3908 promoted the mRNA expression of AdipoR1 in MCF-7 cells, but did not affect the mRNA expression level of SIRT-1, AMPK, and Flotillin-1 (Fig.   2a). [score:7]
The results indicated that miR-3908 inhibited the mRNA expression of AdipoR1 in MCF-7 cells (Fig.   2a), as well as the protein expression of AdipoR1 (Fig.   2b). [score:7]
Furthermore, the inhibitors of miR-3908 promoted the mRNA expression of AdipoR1 in MCF-7 cells, but did not affect the mRNA expression of AMPK, SIRT-1, and Flotillin-1 (a). [score:7]
miR-3908 suppresses the expression of AdipoR1 and its downstream pathway genes, including AMPK, p-AMPK, and SIRT-1. miR-3908 enhances the process of breast cancer cell clonogenicity. [score:5]
Fig. 2Expression of AdipoR1 was suppressed by miR-3908 in MCF-7 cells. [score:5]
Furthermore, miR-3908 did not affect the mRNA expression of AMPK, SIRT-1, and Flotillin-1, but the protein expression of AMPK, p-AMPK, SIRT-1, and Flotillin-1 also decreased. [score:5]
Fig. 1Expression of AdipoR1 was suppressed by miR-3908 in MCF-7 cells. [score:5]
Moreover, miR-3908 did not affect the mRNA expression of AMPK, SIRT-1, and Flotillin-1, but the protein expression of AMPK, p-AMPK, SIRT-1, and Flotillin-1 also decreased (b). [score:5]
Moreover, miR-3908 did not affect the mRNA expression of AMPK, SIRT-1, and Flotillin-1, but the protein expression of AMPK, p-AMPK, SIRT-1, and Flotillin-1 also decreased (Fig.   2b). [score:5]
To explore the anti-invasion functions of miR-3908 inhibitors, the role of these inhibitors on the mobility of AdipoR1 into lipid rafts was determined. [score:5]
Expression of AdipoR1 was suppressed by miR-3908 in MCF-7 cells. [score:5]
The results showed that the relative luciferase activities of AdipoR1 3’-UTR were obviously downregulated in MCF-7 cells transfected with miR-3908 (a), but there was no change in the mut-AdipoR1 group (b). [score:4]
Our work identified that miR-3908 could directly target the mRNAs of AdipoR1. [score:4]
AdipoR1 is a direct target of miR-3908. [score:4]
However, downregulation of miR-3908 facilitated significantly the colony-forming ability of MCF-7 cells. [score:4]
The results showed that the relative luciferase activities of AdipoR1 3’-UTR were obviously downregulated in MCF-7 cells transfected with miR-3908 (Fig.   1a), but there was no change in the mut-AdipoR1 group (Fig.   1b). [score:4]
Then, human breast cancer cell line MCF-7 was cultured in the absence or presence of the mimics or inhibitors of miR-3908, after which the biological functions of MCF-7 cells were analyzed. [score:3]
Our results demonstrated that miR-3908 inhibitors reduced the migration of AdipoR1 into fractions of the lipid raft. [score:3]
These results demonstrated that miR-3908 suppressed the proliferation of MCF-7 cells, lowered its colony formation, and restrained its ability to influence cell migration. [score:3]
Within these miRNAs, miR-3908 potentially co -targeted mRNAs of AdipoR1 3’-UTRs. [score:3]
These results suggested that miR-3908 suppresses the migration of MCF-7 cells. [score:3]
Within these miRNAs, miR-3908 potentially co -targeted the mRNAs of AdipoR1 3’-UTRs. [score:3]
The inhibitors of miR-3908 were as follow: 5’-GUGGUCACCAUCUUCCCUU-3’. [score:3]
Conversely, using the inhibitors of miR-3908, the migration ability was enhanced in MCF-7 cells (a and b). [score:3]
Our results demonstrated that miR-3908 inhibitors reduced the mobility of AdipoR1 into the fractions of the lipid raft. [score:3]
Our findings suggest that targeting miR-3908 and the lipid raft, may be a promising strategy for the treatment and prevention of breast cancer. [score:3]
These results suggested that miR-3908 suppresses the migration ability and invasion of MCF-7 cells. [score:3]
The phenomenon could be enhanced by miR-3908, but reversed by inhibitors of miR-3908 as well as by Flotillin-1 (Fig.   6). [score:3]
Subsequently, MCF-7 cells were exposed to the mimics or inhibitors of miR-3908, and then the cell functions of MCF-7 cells, such as proliferation, colony formation, and migration, were analyzed. [score:3]
To verify the miR-3908 effect on the mRNA and protein expression of AdipoR1, AMPK, SIRT-1, and Flotillin-1 in MCF-7 cells, we accomplished relative quantification analyses with qRT-PCR and Western blots, respectively. [score:3]
AdipoR1 protein interacted with Flotillin-1. The inhibitors of miR-3908 induced mobility of AdipoR1 into lipid rafts. [score:3]
For evaluating the overexpressed or underexpressed possible biotic outcomes induced by miR-3908, several functional experiments were performed in MCF-7 cells. [score:3]
The overlaid image indicates that AdipoR1 overlapped with Flotillin-1 at the MCF-7 cell membrane (b) Fig. 6 The inhibitors of miR-3908 induced the mobility of AdipoR1 into lipid rafts. [score:3]
Our findings suggest that targeting miR-3908 and the lipid raft, being involved in BC cell migration, is a hopeful method for the prevention and treatment of BC. [score:3]
These results demonstrated that miR-3908 suppressed the proliferation of MCF-7 cells. [score:3]
miR-3908 suppresses migration of MCF-7 cells. [score:3]
The miR-3908 was cloned into the open-code frame vector using a DynaExpress miRNA Cloning Kit based on its manufacturer’s instructions, and then modified. [score:3]
For evaluating the possible biotic outcomes induced by miR-3908, we overexpressed or underexpressed miR-3908, and then performed a few functional experiments related to the molecular functions of MCF-7 cells. [score:3]
We found that miR-3908 is expressed in the human breast cancer cell line MCF-7. Adiponectin (APN), an adipokine produced by adipocytes, has been shown to play a critical role in the pathogenesis of obesity -associated malignancies. [score:3]
The phenomenon could be enhanced by miR-3908, but reversed by inhibitors of miR-3908 as well as by Flotillin-1 In the last few years, many researches have indicated that functional receptors assemble at the platforms provided by lipid rafts. [score:3]
Conversely, using the inhibitors of miR-3908, the migration ability was enhanced in MCF-7 cells (Fig.   4). [score:3]
miR-3908 suppresses cell growth and clonogenicity in MCF-7 cells. [score:3]
Moreover, the inhibitors of miR-3908 accentuated the same process of MCF-7 cells (Fig.   3a). [score:3]
Moreover, the inhibitors of miR-3908 accentuated the same process in MCF-7 cells (a). [score:3]
However, it was identified that miR-3908 could not form direct bonds with AMPK (Fig.   1c), SIRT-1 (Fig.   1d), or Flotillin-1 (Fig.   1e) 3’-UTRs, respectively. [score:2]
miR-3908 inhibited significantly the migration ability of MCF-7 cells compared to control (NC) (a and b) in vitro (P < 0.001). [score:2]
Lipid rafts regulate the interactions between AdipoR1 and Flotillin-1 and then the migration process associated with miR-3908 in MCF-7 cells. [score:2]
Compared with control cells, proliferation of MCF-7 cells (Fig.   3a) would be inhibited when they were transfected with miR-3908. [score:2]
miR-3908 inhibited significantly the migration ability of MCF-7 cells compared to control in vitro (Fig.   4; P < 0.001). [score:2]
miR-3908 exerts its effects on the proliferation and migration of MCF-7 cells, which are mediated by lipid rafts regulating AdipoR1’s ability to bind Flotillin-1. miR-3908 is a crucial mediator of the migration process in breast cancer cells. [score:2]
Moreover, it was identified that miR-3908 could not form direct bonds with AMPK, SIRT-1, or Flotillin-1 3’-UTRs, respectively. [score:2]
However, it was identified that miR-3908 could not form direct bonds with AMPK (c), SIRT-1 (d), or Flotillin-1 (e) 3’-UTRs, respectively. [score:2]
In particular, the cell migration effects of miR-3908 have been associated with the regulation of the lipid raft and the AdipoR1-AMPK/SIRT-1 signaling pathway. [score:2]
Lipid rafts regulate the interactions between AdipoR1 and Flotillin-1, and then the migration process associated with miR-3908 in MCF-7 cells. [score:2]
Compared with control cells, proliferation of MCF-7 cells (a) would be suppressed by transfection with miR-3908. [score:2]
Transfection with mimics of miR-3908 was performed using Lipofectamine 3000 (Sigma, Palo Alto, CA, USA) based on the manufacturer’s protocol. [score:1]
org/), confirmed that the 3’-UTR site of AdipoR1 mRNA is complimentary to miR-3908. [score:1]
miR-3908 has effects on the biological functions of MCF-7 cells such as cell proliferation, colony formation, and migration. [score:1]
A further proof experiment was carried out with a luciferase reporter gene assay to identify whether 3’-UTRs of AdipoR1 were bonded directly with miR-3908. [score:1]
Furthermore, the colony formation assay revealed that miR-3908 played a significant role in the suppression of this ability compared with the control group in MCF-7 cells. [score:1]
Additionally, the complementary region to the seed region of the miR-3908 sequence located in positions 139–146 of human AdipoR1 3’-UTR, CAUUGCUA. [score:1]
We identified the expression pattern of miR-3908 in MCF-7 cells according to the TaqMan miRNA assays with its specific primers. [score:1]
AdipoR1 may control the migration of MCF-7 cells mediated by the lipid raft through regulating the interaction between AdipoR1 and Flotillin-1. We, therefore, investigated the effect of miR-3908 on regulating the interaction between AdipoR1 and Flotillin-1 in MCF-7 cells. [score:1]
To confirm the prediction that miR-3908 is matched with AdipoR1, we used 3’-UTR luciferase activity of AdipoR1 to assess this. [score:1]
Then, either negative control (NC) or miR-3908 were co -transfected into cells. [score:1]
These results suggested that miR-3908 also lowered colony formation of MCF-7 cells (Fig.   3b) (P < 0.001). [score:1]
qRT-PCR was used to identify the dose effect of miR-3908. [score:1]
To assess the role of miR-3908 in human MCF-7 cells, we first identified whether miR-3908 sequences are present in AdipoR1 mRNA. [score:1]
The results of luciferase reporter analysis indicated that the relative activity of AdipoR1 3’-UTR significantly decreases in MCF-7 cells transfected with miR-3908, but there were no changes in the mut-AdipoR1 group. [score:1]
The mimics of miR-3908 were as follows: sense 5’-AAGGGAAGAUGGUGACCACUU-3’ and antisense 5’-AAGUGGUCACCAUCUUCCCUU-3’. [score:1]
These results suggested that miR-3908 also lowered colony formation of MCF-7 cells (b) (P < 0.001). [score:1]
In summary, we have illustrated miR-3908, which specifically binds to AdipoR1 mRNA 3’-UTR. [score:1]
A further proof experiment was carried out with a luciferase reporter gene assay, to identify whether 3’-UTRs of AdipoR1 were bonded directly with miR-3908. [score:1]
The mimics of miR-3908 and transfection. [score:1]
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