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28 publications mentioning hsa-mir-802

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-802. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 263
Other miRNAs from this paper: hsa-mir-10b, hsa-mir-203a, hsa-mir-203b
The present article provides evidence, for the first time, that miR-802 expression is down-regulated in human PCa tissues and cells, and miR-802 could suppress EMT of PCa cells through directly inhibiting Flotillin-2 (Flot2), a member from flotillin family that serves an important role in the pathogenesis and progression of human malignancies [13]. [score:11]
The present study revealed that mesenchymal markers, such as N-cadherin and vimentin, were down-regulated, but epithelial cell markers, such as E-cadherin were up-regulated in PCa cells overexpressing miR-802, indicating that miR-802 suppresses EMT. [score:11]
The results demonstrated that compared with control cells, up-regulation of miR-802 could significantly suppress DU145 cell migration and invasion (Figure 6), and these effects were obviously restored by Flot2 overexpression, clearly indicating that miR-802 can inhibit the migratory and invasive phenotype of PCa cells by regulating Flot2. [score:10]
Figure 4 miR-802 suppresses Flot2 expression by targeting the 3′-UTR of Flot2 mRNA(A) The seed sequences for miR-802 in the 3′-UTR of Flot2 revealed by TargetScan analysis. [score:9]
Our findings revealed that overexpression of miR-802 in PCa cells dramatically inhibits cell proliferation, migration and invasion in vitro, which raises the possibility for the development of miR-802 as a potent target for novel, promising therapies for the highly aggressive and malignant PCa in clinical application. [score:8]
miR-802 suppresses Flot2 expression by targeting the 3′-UTR of Flot2 mRNA. [score:7]
miR-802, a miRNA located on chromosome 21, is found to be significantly decreased in human breast cancer tissues and inhibit cell proliferation through suppressing Forkhead box protein M1 (FoxM1) expression [11]. [score:7]
These results suggested that miR-802 directly regulated Flot2 expression by targeting 3′-UTR of its mRNA. [score:7]
miR-802 directly targets Flot2 in PCa cellsIt is wi dely acknowledged that miRNAs exert their functions through modulation of target mRNAs. [score:6]
Therefore, we considered that decreased Flot2 expression induced by overexpressed miR-802 might be critical in suppressing PCa metastasis associated with TGF-β -mediated EMT. [score:6]
Down-regulation of miR-802 correlates with PCa metastasisTo investigate the expression pattern and clinicopathologic significance of miR-802 in PCa, we first detected the expression and clinical values of miR-802 in 73 cases of paired PCa tissue samples. [score:6]
Figure 5 miR-802 suppresses EMT in PCa cells by regulating Flot2Western blot was performed to detect the expression of E-cadherin, N-cadherin, and Vimentin proteins in DU145 cells. [score:6]
Consistently, our results demonstrated that up-regulation of miR-802 in PCa cells significantly inhibits cell proliferation, migration and invasion. [score:6]
In osteosarcoma, however, miR-802 expression was found to be remarkably up-regulated in tumor tissues [24]. [score:6]
As shown in Figure 4C,D, Flot2 expression was significantly reduced in miR-802 mimics -transfected DU145 cells whatever the mRNA or protein levels (all P<0.05), and down-regulation of miR-802 had the opposite effects in RWPE-1 cells (all P<0.05). [score:6]
To analyze the clinicopathological significance of miR-802, the mean fold change of miR-802 expression (0.27) was considered as a cut-off value to categorize all 73 PCa patients into two groups: an miR-802 low expression group (n=27) and an miR-802 high expression group (n=46). [score:6]
Figure 1 miR-802 expression was reduced in PCa tissues and cell lines(A) Relative expression of miR-802 in 73 pairs of PCa tissues and matched adjacent non-tumor tissues. [score:5]
Similarly, the average tumor weight was remarkably reduced by miR-802 overexpression (P<0.05, Figure 3B,C), further indicating that miR-802 might suppress tumor growth in vivo. [score:5]
miR-802 inhibits in vivo PCa tumor growthTo further explore the function of miR-802 on tumor growth in vivo, DU145 cells with overexpressed miR-802 were generated and injected subcutaneously into the dorsal flank of nude mice to establish DU145 tumor xenografts. [score:5]
Overexpression Flot2 plasmid pcDNA3.1-Flot2, miR-802 mimics, miR-802 inhibitor and their control miRNA oligonucleotides (miR-Con, anti-miR-Con) were acquired from GenePharm (Shanghai, China) and transfected into the cells with Lipofectamine™ 2000 transfection reagent (Invitrogen) according to the manufacturer’s instructions. [score:5]
The associations between miR-802 expression and the clinical features of PCa patients were documented in Table 1. miR-802 expression was observed to be correlated closely with Gleason score (P=0.004), distant metastasis (P=0.002) and pathological stage (P=0.02). [score:5]
Overexpression of miR-802 significantly inhibited cell proliferation in DU145 cells compared with the control groups, as demonstrated by (P<0.05, Figure 2A). [score:4]
To illustrate that the endogenous miR-802 can regulate the expression of Flot2, miR-802 mimics was transfected into DU145 cells. [score:4]
Müller et al. [12] speculated that down-regulation of miR-802 might lead to increased Wnt activity in pancreatic ductal adenocarcinoma. [score:4]
miR-802 directly targets Flot2 in PCa cells. [score:4]
Down-regulation of miR-802 correlates with PCa metastasis. [score:4]
In addition, site-directed mutagenesis of the seed region dramatically reversed the inhibitory function of miR-802 on firefly luciferase activity (Figure 4B). [score:4]
As demonstrated in Figure 5, reduced protein levels of mesenchymal markers (vimentin and N-cadherin) were found in miR-802 mimics -transfected DU145 cells compared with that in control cells (all P<0.05), and epithelial marker (E-cadherin) protein expression was elevated in DU145 cells with overexpressed miR-802 (P<0.05). [score:4]
Moreover, up-regulation of miR-802 greatly increased the number of apoptotic PCa cells than control miR -transfected cells, as shown by flow cytometry (P<0.05, Figure 2B). [score:4]
miR-802 suppresses EMT in PCa cells by regulating Flot2. [score:4]
miR-802 suppresses cell migration and invasion in PCa cells in vitro by regulating Flot2. [score:4]
The relative expression of miR-802 was illustrated as fold difference relative to U6. [score:3]
The luciferase vectors and miR-802 -expressing vector were co -transfected in DU145 cells by using Lipofectamine™ 2000 (Invitrogen). [score:3]
Taken together, our data revealed that miR-802 suppresses EMT in PCa cells in vitro. [score:3]
The article of Li et al. [23] indicated that decreased miR-802 expression might play a critical role in the carcinogenesis and metastasis of pulmonary cells induced by long-term exposure to PM 2.5. [score:3]
miR-802 suppresses cell migration and invasion in PCa cells in vitro by regulating Flot2The effect of miR-802 on the migration and invasion of PCa cells was determined through transwell assay. [score:3]
With bioinformatics prediction, it was identified that Flot2 is the theoretical target of miR-802. [score:3]
miR-802 suppresses cell proliferation and promotes apoptosis in PCa cells in vitroFunction assays were performed to ascertain whether miR-802 could regulate cell proliferation and apoptosis in PCa. [score:3]
Our data suggested that aberrant miR-802 expression is significantly correlated to distant metastasis in PCa patients. [score:3]
org) [16], we have identified that Flot2 is a potential target gene of miR-802. [score:3]
miR-802 suppresses cell proliferation and promotes apoptosis in PCa cells in vitro. [score:3]
miR-802 expression was remarkably decreased in PCa tissues than in corresponding adjacent non-tumor mucosa (Figure 1A, P<0.05). [score:3]
Besides, the repressive effects of miR-802 on EMT were obviously restored by Flot2 overexpression. [score:3]
To investigate the expression pattern and clinicopathologic significance of miR-802 in PCa, we first detected the expression and clinical values of miR-802 in 73 cases of paired PCa tissue samples. [score:3]
Figure 3 miR-802 inhibits in vivo PCa tumor growth(A) The growth curves were plotted to monitor tumor volumes for 5 weeks. [score:3]
miR-802 expression was reduced in PCa tissues and cell lines. [score:3]
miR-802 expression was determined by qRT-PCR and normalized against U6. [score:3]
To further explore the function of miR-802 on tumor growth in vivo, DU145 cells with overexpressed miR-802 were generated and injected subcutaneously into the dorsal flank of nude mice to establish DU145 tumor xenografts. [score:3]
miR-802 inhibits in vivo PCa tumor growth. [score:3]
In turn, experimental validation demonstrated that Flot2 is a bona fide target of miR-802 in PCa cells. [score:3]
A mutant construct specific for putative miR-802 binding site in Flot2 3′-UTR was also generated using Quick Change Site-Directed Mutagenesis Kit (Angilent). [score:2]
miR-802 suppresses EMT in PCa cells by regulating Flot2In order to verify whether miR-802 can modulate EMT in PCa cells, we investigated several common EMT markers through analysis. [score:2]
Intriguingly, the regulatory function of miR-802 in carcinogenesis remains controversial. [score:2]
The tumor growth was markedly slower in mice injected with DU145 cells overexpressing miR-802 compared with those in control mice (P<0.05, Figure 3A). [score:2]
In addition, miR-802 expression was evaluated in two types of PCa cell lines (PC3 and DU145 cells) and normal prostate cells (RWPE-1). [score:1]
Figure 2 miR-802 suppresses cell proliferation and promotes apoptosis in PCa cells in vitro(A) Cell proliferation in DU145 cells was evaluated through. [score:1]
To date, however, little is understood about the clinical significance and biological functions of miR-802 in human PCa. [score:1]
Statistical significance was determined by a two-tailed Student’s t test: * P<0.05 in comparison with miR-Con, [#] P<0.05 in comparison with miR-802. [score:1]
For the subcutaneous xenograft mouse mo del, DU145 cells (5 × 10 [6]) that were transiently transfected with miR-802 mimics or miR-Con were suspended in 100 µl medium and subcutaneously injected into the left and right backside flanks of nude mice (n=5 mice/group) respectively. [score:1]
Figure 6 miR-802 suppresses cell migration and invasion in PCa cells in vitro by regulating Flot2Transwell assay was performed to investigate the migratory and invasive capacities of DU145 cells. [score:1]
Statistical significance was determined by a two-tailed Student’s t test: * P<0.05 in comparison with miR-Con; [#] P<0.05 in comparison with miR-802. [score:1]
Function assays were performed to ascertain whether miR-802 could regulate cell proliferation and apoptosis in PCa. [score:1]
The binding sites of miR-802 were predicted at positions 82–89 in the 3′-UTR of Flot2 mRNA, as demonstrated in Figure 4A. [score:1]
We transfected DU145 PCa cells with miR-802 mimics or control miRNA, and then explored the proliferation and apoptosis of cell lines. [score:1]
Accordingly, it is necessary to further clarify the contribution of miR-802 in multiple malignancies in the near future. [score:1]
DU145 cell line exhibited the lowest miR-802 level and was thus selected for further trials. [score:1]
As illustrated in Figure 1B, after normalization to U6, the mRNA levels of miR-802 were evidently reduced in two types of PCa cell lines (PC3 and DU145 cells) than that in normal prostate cells (RWPE-1). [score:1]
Our results revealed that miR-802 might function as a potential therapeutic strategy in metastatic cancers. [score:1]
To draw a conclusion, this might be the first study to identify miR-802 as a novel potential oncogene in PCa through induction of an EMT program. [score:1]
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2
[+] score: 45
They demonstrated that miR-802 modulated the 3′UTR of caveolin-1 (luciferase activity) and the miR-802 “sponge” increased the expression of endogenous cavelolin-1 (immunoblot), providing evidence that miR-802 reduced expression of caveolin-1. Since miR-802 regulated the expression of caveolin-1, they hypothesized that a high K [+] diet would result in reduced caveolin-1 expression. [score:10]
Further, to determine if the expression of caveolin-1 reduced the amount of K [IR]1.1 at the membrane, the authors provided functional data, with patch-clamp experiments, that co -expression of caveolin-1 and K [IR]1.1 caused a large decrease in K [+] current when compared to K [+] current of cells not transfected with caveolin-1. Finally, with a combination of perforated whole cell experiments with HEK cells, Lin et al. (2011) reported that co-transfection of K [IR]1.1 and pre-miR-802 or K [IR]1.1 + pre-miR-802 + caveolin-1 for 24 h resulted in that (i) pre-miR-802 increased K [+] currents of K [IR]1.1, (ii) the effect of miR-802 on K [+] currents was due to decreased expression of caveolin-1, since expression of mutant caveolin-1 (missing 3′UTR) reduced the effect of pre-miR-802 and decreased the K [+] currents, and (iii) in M1-cells, miR-802 stimulated the surface expression of K [IR]1.1. [score:10]
Lower Panel: miR-802 inhibits caveolin 1 which relieves the inhibition of K [IR]1.1 by caveolin 1 and increases K [IR]1.1. [score:5]
miR-802 and K [IR]1.1. miR-194 and K [IR]1.1. miR-205 suppresses K [IR]4.1 (KCNJ10) in corneal epithelial cells. [score:3]
Therefore, miR-802 increased the surface expression of K [IR]1.1, by reducing caveolin-1 that increased the activity of K [IR]1.1 (Figure 2A). [score:3]
Thereafter, Lin et al. (2011) turned their efforts to linking miR-802 and caveolin-1 in the regulation of K [IR]1.1. [score:2]
MiR-802 and miR-194 increase K [IR]1.1 (KCNJ1) abundance in the kidney by indirect pathways. [score:2]
As with miR-802, Wang and coworkers (Lin et al., 2014) used a similar high K [+] diet experimental approach to investigate the role of miR-194 in the regulation of K [IR]1.1 by targeting intersectin 1 (ITSN1). [score:2]
The authors used multiple approaches to determine the role of miR-802 in the regulation of K [IR]1.1. [score:2]
Using Northern blot and PCR experiments, they demonstrated that miR-802 was elevated in the kidney of mice fed a high K [+] diet. [score:1]
Therefore, Lin et al. (2011) established that miR-802 was present in the mouse CCDs and the miR was modulated by high K [+] diet. [score:1]
One miR identified was miR-802. [score:1]
The authors used human embryonic kidney (HEK) cell line, a caveolin-1 mutant 3′UTR and a microRNA-sponge (to “absorb” the mature form of miR-802) approach. [score:1]
After which, Lin et al. (2011), used databases and identified that the 3′UTR of caveolin-1 contained a recognized binding site for miR-802. [score:1]
Additionally, using qRT-PCR, they reported increased levels of pre-miR-802 in CCDs isolated from mice fed a high K [+] diet. [score:1]
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3
[+] score: 36
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-34a, hsa-mir-182, hsa-mir-210, hsa-mir-215, hsa-mir-221, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-144, hsa-mir-127, hsa-mir-1-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-375, hsa-mir-133b, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-486-1, bta-mir-26a-2, bta-let-7f-2, bta-mir-16b, bta-mir-20a, bta-mir-21, bta-mir-221, bta-mir-34b, bta-mir-127, bta-mir-15b, bta-mir-20b, bta-mir-215, bta-mir-210, bta-let-7f-1, bta-mir-122, bta-mir-34c, bta-mir-34a, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-141, bta-mir-144, bta-mir-16a, bta-mir-182, bta-mir-26a-1, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-486, bta-mir-2285a, bta-mir-2285d, bta-mir-2285b-1, bta-mir-2376, bta-mir-2285c, bta-mir-1388, bta-mir-3431, hsa-mir-451b, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2285n-7, bta-mir-2285k-2, bta-mir-6529a, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2285k-5, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, hsa-mir-486-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-6529b, bta-mir-133c, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2285ae, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm, hsa-mir-6529
Of note, the human homologue of miR-802 was distinctly enriched in liver, where its expression was 87-fold higher than the mean expression across all tissues, and 5.2-fold higher than in intestine, the tissue with the second highest mean expression levels (Fig. 5c). [score:7]
Specifically, hepatic levels of miR-802 were elevated in obese individuals, contributing to insulin insensitivity, glucose intolerance and increased hepatic gluconeogenesis by downregulation of HNF1B [44]. [score:4]
Another study identified miR-802 as a target of constitutive androstane receptor (CAR) signalling, which is involved in the regulation of xenobiotic detoxification, lipid homeostasis and energy metabolism [46]. [score:4]
Interestingly, serum miR-802 levels were reportedly increased in type 2 diabetes patients providing a potential circulating biomarker for this disease [45]. [score:3]
Expression profiling of selected plasma-enriched miRNAs across different bovine tissues revealed miR-802, a previously unidentified bovine miRNA, to be highly enriched in liver. [score:3]
Circulating microRNA miRNA Liver Tissue-specific Tissue-enriched Biomarker Cow miR-802 MicroRNAs (miRNAs) are short, non-coding RNA molecules which are primarily involved in the post-transcriptional fine-tuning of gene expression [1]. [score:3]
In particular, miR-802, a circulating miRNA not previously identified in cattle, can reportedly regulate insulin sensitivity and lipid metabolism, and thus could potentially provide a specific biomarker of liver function, a key parameter in the context of post-partum negative energy balance in dairy cows. [score:2]
Overall, these results highlight the importance of miR-802 in the regulation of glucose and lipid metabolism as well as xenobiotic responses in the liver. [score:2]
Although not previously reported in cow, data in humans and mice have shown miR-802 to be a key a regulator of liver function. [score:2]
Using BLAT (UMD3.1, accessed 27/07/16) we mapped the mature miR-802 sequence to bovine chromosome 1 (chr1: 149720302–149,720,392 [+]). [score:1]
These analyses revealed 10 miRNAs which either were present in bovine but not in human (miR-1388-5p, miR-1388-3p, miR-2376, miR-2285 t, miR-3431 and miR-6529a, Fig. 5b) or were homologues of human miRNAs not identified previously in cow (miR-210-3p, miR-802, miR-4532 and miR-4792, Fig. 5c). [score:1]
Indeed, this location in the bovine genome has been annotated as a novel miRNA with a secondary structure that matches miR-802. [score:1]
Furthermore, circulating miR-802 has been proposed as a biomarker of drug -induced liver damage in rats, with an observed increase in miRNA levels in response to tissue damage being comparable to that of the liver-enriched miR-122 [47, 48]. [score:1]
Using next-generation sequencing, we provide a list of potential tissue-enriched miRNAs in circulation including miR-802, a previously uncharacterised bovine liver-specific miRNA which may prove useful as a disease biomarker in high-producing cows. [score:1]
Profiling of additional miRNAs across different tissues identified the human homologue, miR-802, as highly enriched specifically in liver. [score:1]
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4
[+] score: 32
Eight miRNAs (miR-101, miR-107, miR-122, miR-29, miR-365, miR-375, miR-378, and miR-802), whose expression was found to be downregulated in c-Myc and/or AKT/Ras liver tumors, were selected and their tumor suppressor activity was assessed in c-Myc and AKT/Ras mice. [score:8]
miRNA Oncogene Growth Inhibition miR-101 c-Myc +++ AKT/Ras +++ miR-107 c-Myc + AKT/Ras ++ miR-122 c-Myc ++ AKT/Ras ++ miR-29 c-Myc ++ AKT/Ras + miR-365 c-Myc ++ AKT/Ras ++ miR-375 c-Myc + AKT/Ras +++ miR-378 c-Myc − AKT/Ras − miR-802 c-Myc ++ AKT/Ras − Taken together, the present results indicate that miR-378 does not possess tumor suppressor activity on c-Myc and AKT/Ras induced hepatocarcinogenesis in mice. [score:5]
miRNA Oncogene Growth Inhibition miR-101 c-Myc +++ AKT/Ras +++ miR-107 c-Myc + AKT/Ras ++ miR-122 c-Myc ++ AKT/Ras ++ miR-29 c-Myc ++ AKT/Ras + miR-365 c-Myc ++ AKT/Ras ++ miR-375 c-Myc + AKT/Ras +++ miR-378 c-Myc − AKT/Ras − miR-802 c-Myc ++ AKT/Ras − Taken together, the present results indicate that miR-378 does not possess tumor suppressor activity on c-Myc and AKT/Ras induced hepatocarcinogenesis in mice. [score:5]
In summary, the present results indicate that miR-107, miR-122, miR-29, miR-365, and miR-802 possess weak to moderate tumor suppressive properties, as none of them is able to completely prevent oncogene driven liver tumor development in mice. [score:4]
Weak to moderate tumor suppressor potential of miR-107, miR-122, miR-29, miR-365, and miR-802 in c-Myc and AKT/Ras driven liver tumor development. [score:4]
Overexpression of miR-802 did not affect AKT/Ras induced liver tumor formation, with all AKT/Ras/miR-802 injected mice being euthanized due to high tumor burden by 8 weeks post injection (Supplementary Figure 8C and 8D). [score:3]
On the other hand, none of c-Myc/miR-802 injected mice showed enlarged liver by 8 weeks post injection. [score:1]
Histologically, all c-Myc/miR-802 injected mice developed liver tumors, although the tumor burden was much lower than that of c-Myc/pT3 mice. [score:1]
Histologically, tumors developed in c-Myc/miR-802 mice were hepatoblastomas, identical to c-Myc/pT3 tumors (Supplementary Figure 8A and 8B). [score:1]
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5
[+] score: 27
Based on this analysis, we concluded that miR-802 was not highly expressed in the xenografts and was not differentially expressed between normal and tumor samples. [score:5]
Capture of mature miRNAs was performed using the following chimeric hairpin target capture oligonucleotides (TCO) [20]: for miR-21 (TTTTTTTTTTTTUCAACAUCAGUCUGAUAAGCUAAAAAAAAAAAAA), for miR-182 (TTTTTTTTTTTTAGUGUGAGUUCUACCAUUGCCAAAAAAAAAAAAAAA), for miR-221 (TTTTTTTTTTTTGAAACCCAGCAGACAAUGUAGCUAAAAAAAAAAAA), for miR-222 (TTTTTTTTTTTTACCCAGUAGCCAGAUGUAGCUAAAAAAAAAAAA), and for miR-802 (TTTTTTTTTTTTACAAGGAUGAAUCUUUGUUACUGAAAAAAAAAAAA). [score:3]
The human pre-miR-802 sequence was obtained from the miRBase [17] of the Sanger Institute and a synthetic hairpin precursor was synthesized using PCR amplification of the 94 nt pre-mir-802 sequence from LNCaP genomic DNA cloned into pBluescript II SK (+) and expressed as an in vitro transcript. [score:3]
B) Specificity of the miR-221 assay using the corresponding synthetic miR-221 target as compared to synthetic miR-222, miR-30b, and miR-802 targets. [score:3]
The authors thank Irene Andruszkiewicz for cloning and expression of the pre-miR-802 in vitro transcript and Maren Spillane, Abby Rynko, Michael Barcas, Julie Haase, and Joel Brothers for oligonucleotide synthesis. [score:3]
This mo del system demonstrated that 5 copies per reaction of this particular intended target, miR-802, could be detected above nonspecific background signals. [score:3]
C) Calibration chart for the amplification curves in B. D) Calibration chart for the miR-802 assay tested on various copy number input of mature target vs. [score:2]
B) Amplification curves from tests of the miR-802 assay on various input copy numbers of synthetic miRNA targets. [score:2]
We selected miR-802, which resides in chromosomal region 21q22.12, due to its proximity to the TMPRSS2:ERG gene fusion. [score:1]
The specificity of our miR-221 assay was demonstrated using other synthetic mature miRNAs as targets (Figure 4B), analogous to our previous demonstration for the miR-802 assay (previous section). [score:1]
pre-miR-802 transcript. [score:1]
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6
[+] score: 16
On the other hand, miR-802 was investigated in mice by using expression and sequencing studies [28] and Kuhn et al. used miRNA expression profiling, miRNA RT-PCR and miRNA in situ hybridization experiments to identify miR-802 was up-regulated in fetal brain and heart specimens from individuals with Down syndrome when comparing with control groups [29]. [score:6]
However, previous study reported endogenous miR-802 was not detected in breast cancer patients based on miRNA expression profiles [27]. [score:3]
According to these, miR-802 is expressed in other tissues, but not in breast tissues. [score:3]
Thus, the expression levels of miR P-27-5p and miR-802 in breast tissues are different. [score:3]
Our previous report suggested that miR P-27-5p may be an alternative mature form of miR-802 [6]. [score:1]
[1 to 20 of 5 sentences]
7
[+] score: 13
In vitro, expression of miR-802 suppressed the expression of caveolin-1; in vivo, the level of miR-802 was inversely correlated with that of caveolin-1 [50]. [score:7]
Caveolin-1 is the molecular target of miR-802 in the collecting duct. [score:3]
High K [+] intake stimulated the transcription of miR-802, which in turn decreased the expression of caveolin-1 and increased the membrane localization of ROMK, leading to higher K [+] excretion (Figure 4) [50]. [score:3]
[1 to 20 of 3 sentences]
8
[+] score: 13
Other miRNAs from this paper: hsa-mir-99a, mmu-mir-99a, mmu-mir-155, hsa-mir-155, mmu-mir-802
In DS neurons, overexpression of miR-155 and miR-802 inhibited the expression of the target, methyl-CpG -binding protein 2 (MeCP2) [107]. [score:9]
In T21 AF-iPSC-NPCs, the investigators found that the expression levels of miR-155 and miR-802 were highly elevated and there was low expression of methyl-CpG -binding protein 2 (MeCP2) and thus this reflected the observations in DS neurons [106]. [score:3]
The syndrome is caused by an extra duplication of chromosome 21, which harbors miRNAs including miR-99a, miR-155, and miR-802 [51]. [score:1]
[1 to 20 of 3 sentences]
9
[+] score: 11
miR-802, co-expressed with RUNX, targets multiple pathway genes: IFN-γ, NFY-C, CANX, and the HLA-DM complex. [score:5]
The HLA-DM protein, another chaperone, finally, is targeted by both miR-802 and miR-577. [score:3]
STAT1 is responsible for the transcription of two PAGs (1) RUNX and (2) UGT8, that respectively co-express miR-802 and miR-577, responsible for the loop closure. [score:3]
[1 to 20 of 3 sentences]
10
[+] score: 10
Disease Origin References of iPSC lines Phenotype of iPSC-derived neurons miRNAs of interest Fragile X syndrome Loss of function of FMRP (FMR1 gene) Urbach et al. (2010), Sheridan et al. (2011) Hyper-excitability of glutamatergic synapses DICER and AGO-1 complexes Rett’s syndrome Loss of function of MeCP2 transcriptional repressor Marchetto et al. (2010), Kim et al. (2011c), Cheung et al. (2012) Decreased soma size, neurite atrophy, decreased efficiency of glutamatergic synapses miR-132, miR-184, miR-483-5p, miR-212 Schizophrenia Multifactorial Urbach et al. (2010); Brennand et al. (2011), Paulsen Bda et al. (2012), Robicsek et al. (2013) Diminished neuronal connectivity miR-17-5p, miR-34a, miR-107, miR-122, miR-132, miR-134, miR-137 Down’s syndrome Additional copy of chromosome 21 Briggs et al. (2013), Weick et al. (2013) Reduced synaptic activity, increased sensitivity to oxidative stress miR-99a, miR-125b, miR-155, miR-802, Ret 7c Micro -RNAs, as fine regulators of protein translation, influence directly the level of gene expression. [score:9]
Hsa21 has been predicted to contain at least five nc -RNAs, miR-99a, miR-125b, miR-155, miR-802, and Ret-7c (Kuhn et al., 2008). [score:1]
[1 to 20 of 2 sentences]
11
[+] score: 8
Overexpression of microRNA miR802 led to downregulation of FOXM1 and inhibited proliferation of breast cancer cells [73]. [score:8]
[1 to 20 of 1 sentences]
12
[+] score: 8
Also, overexpression of miR-802 suppresses breast cancer cell proliferation by downregulating FOXM1 [51]. [score:8]
[1 to 20 of 1 sentences]
13
[+] score: 8
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-212, hsa-mir-193a
For instance, miR-16 inhibits cell proliferation by targeting IGF1R and the Raf1-MEK1/2-ERK1/2 pathway in osteosarcoma [20], and miR-802 promotes osteosarcoma cell proliferation by down -regulating the p27 cell-cycle inhibitor [21]. [score:8]
[1 to 20 of 1 sentences]
14
[+] score: 6
Other miRNAs from this paper: mmu-mir-155, hsa-mir-155, mmu-mir-802
MicroRNAs encoded by Hsa21 may also influence development of the brain; specifically trisomy of miR-155 and miR-802 has been suggested to regulate the expression of the methyl-CpG -binding-protein gene (MECP2), which is known to be important in neurodevelopment [65]. [score:6]
[1 to 20 of 1 sentences]
15
[+] score: 5
Cao et al. and Wang et al. revealed that the expression of p27 was negatively regulated by miR-802 and miR-25 40 41, thus illustrating that p27 might be regulated by several miRNAs simultaneously in OS. [score:5]
[1 to 20 of 1 sentences]
16
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Chronic ethanol feeding to mice induces an increase in the expression of miR-21, miR-199a-3p and miR-211 and down regulated miR-148a and miR-802 in the pancreas [18]. [score:4]
[1 to 20 of 1 sentences]
17
[+] score: 4
The miRNAs encoded by hsa 21 (i. e., hsa-miR-99a, let-7c, miR-125b-2, miR-155, and miR-802) have been proven to correlate with the complex and variable phenotypes of DS and were shown to be overexpressed in the heart, frontal cortex, and hippocampus of fetuses with DS as found in our study (4, 16, 17, 18, 19). [score:3]
The expressions of 14 miRNAs [i. e., human chromosome (hsa)-let-7c, hsa-mir-125b-2, hsa-mir-155, hsa-mir-3118, hsa-mir-3156, hsa-mir-3197, hsa-mir-3648, hsa-mir-3687, hsa-mir-4327, hsa-mir-4759, hsa-mir-4760-3p, hsa-mir-548x, hsa-mir-802, and hsa-mir-99a] encoded by chromosome 21 were evaluated; u6-snRNA was used as the control sample for normalization. [score:1]
[1 to 20 of 2 sentences]
18
[+] score: 3
Other miRNAs from this paper: mmu-mir-155, hsa-mir-155, mmu-mir-802
The trisomic region of Mmu16 in Ts65Dn mice harbours two of the miRNAs located on Hsa21, mir-155 and mir-802, [2, 80, 81, 83, 84] and these are overexpressed in Ts65Dn hippocampus and prefrontal cortex [80]. [score:3]
[1 to 20 of 1 sentences]
19
[+] score: 3
The authors specifically quantified and validated changes in neuronal miR-802, a suppressor of caveolin-1 (Lin et al., 2011), in the CSF of control (n = 8) and AD (n = 14) patients. [score:3]
[1 to 20 of 1 sentences]
20
[+] score: 3
Moreover, extra copies of let-7c, miR-99a, -125b-2, -155, and miR-802 on chromosome 21 are also over-expressed in DS patients [106]. [score:3]
[1 to 20 of 1 sentences]
21
[+] score: 3
miR-143a, miR-802, and miR-181a/543 affect hepatic insulin signaling by targeting Oxysterol binding protein like 8 (Orp8), Hepatocyte nuclear factor 1-β (Hnf1β), and Sirtuin 1 (SIRT1), respectively [55, 56, 57, 58]. [score:3]
[1 to 20 of 1 sentences]
22
[+] score: 3
Furthermore, the expression levels of 8 DEMs (i. e., miRNA-1927, miRNA-802-5p, miRNA-6236, miRNA-3968, miRNA-126-5p, miRNA-100-5p, miRNA-5100, and miRNA-3102-3p) were also verified by qRT-PCR (Supplementary Table S5). [score:3]
[1 to 20 of 1 sentences]
23
[+] score: 2
miRNAs play an essential role in the maintenance of insulin signaling and glucose homeostasis and dysregulation of miRNAs (e. g., miR-103, miR-107, miR-802 and the let-7 family) is associated with features of the metabolic syndrome, obesity, and type 2 diabetes in a number of experimental mo dels [115, 116, 117, 118]. [score:2]
[1 to 20 of 1 sentences]
24
[+] score: 1
Bioinformatic analysis has demonstrated that Hsa21 harbors five miRNA genes, miR-99a, let-7c, miR-125b-2, miR-155 and miR-802 (12, 13). [score:1]
[1 to 20 of 1 sentences]
25
[+] score: 1
Other miRNAs from this paper: hsa-mir-155
AF-iPS have also been generated from human second trimester fetuses with trisomy 21 obtaining an in vitro mo del of Down syndrome allowing the mo deling of the neurogenesis in AF-iPS with trisomy 21 and highlighting the role of miR-155 and miR-802, both encoded by chromosome 21, in the impairment of neuronal differentiation [28, 60]. [score:1]
[1 to 20 of 1 sentences]
26
[+] score: 1
These two FSHD1 fetal muscle biopsies share 11 miRNAs with similar modulations (Fig. 4), miR-1225–3p, miR-19b-1*, miR-208b, miR-22, miR-372, miR-383, miR-767–3p, miR-802, miR-872, miR-875–5p, and miR-892b. [score:1]
[1 to 20 of 1 sentences]
27
[+] score: 1
Complete data were available for five miRNAs (miR99a, miR125b, miR155, miR802 and let-7 c). [score:1]
[1 to 20 of 1 sentences]
28
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-25, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, dme-mir-1, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-124-3, mmu-mir-134, mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, dme-mir-92a, dme-mir-124, dme-mir-92b, mmu-let-7d, dme-let-7, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-134, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-92a-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-25, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-92a-1, hsa-mir-379, mmu-mir-379, mmu-mir-412, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-92-1, gga-mir-17, gga-mir-1a-2, gga-mir-124a, gga-mir-10b, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-1a-1, gga-mir-124b, gga-mir-1b, gga-let-7a-2, gga-let-7j, gga-let-7k, dre-mir-10a, dre-mir-10b-1, dre-mir-430b-1, hsa-mir-449a, mmu-mir-449a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-1, dre-mir-17a-2, dre-mir-25, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-412, hsa-mir-511, dre-let-7j, hsa-mir-92b, hsa-mir-449b, gga-mir-449a, hsa-mir-758, hsa-mir-767, hsa-mir-449c, mmu-mir-758, mmu-mir-802, mmu-mir-449c, mmu-mir-105, mmu-mir-92b, mmu-mir-449b, mmu-mir-511, mmu-mir-1b, gga-mir-1c, gga-mir-449c, gga-mir-10a, gga-mir-449b, gga-mir-124a-2, mmu-mir-767, mmu-let-7j, mmu-let-7k, gga-mir-124c, gga-mir-92-2, gga-mir-449d, mmu-mir-124b, gga-mir-10c, gga-let-7l-1, gga-let-7l-2
The results showed that hsa-mir-758 can be assigned to the hsa-mir-379,380, 411 family; hsa-mir-767 can be assigned to the hsa-mir-105 family; and hsa-mir-802 can be assigned to the hsa-mir-511 family. [score:1]
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