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70 publications mentioning hsa-mir-365a

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-365a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 275
Other miRNAs from this paper: hsa-mir-127, hsa-mir-365b, hsa-mir-558
It was also reported that miR-365 regulates IL-6 expression via the MAPK/ERK pathway in HEK293 and Hela cells, while enhanced expression of IL-6 in macrophages of patients with pulmonary tuberculosis is associated with downregulation of miR-365 44, 45. [score:9]
MiR-365 expression was markedly suppressed in OA compared to normal cartilage, and was shown to actively suppress the expression of various HIF-2α-regulated catabolic factors in chondrocytes. [score:8]
miR-365 suppressed IL-1β -mediated catabolic responses in monolayer and 3D culture of articular chondrocytes, with concurrent regulation of HIF-2α expression, suggesting that miR-365 could be a useful target for OA therapy. [score:8]
Pre-treatment with these inhibitors significantly attenuated the effects of IL-1β on miR-365 down-regulation, restoring its expression to levels at those of untreated control (Fig.   3B). [score:8]
Considering the role of HIF-2α in the regulation of cartilage degradation, these data strongly implicate miR-365 as a potential therapeutic target for the treatment of OA, though significant obstacles still remain in terms of miRNA delivery and possible off-target effects due to redundant biological targets of a single miRNA. [score:8]
Hydrostatic pressure suppressed the expression of miR-365 and downregulation of HDAC4 in OA chondrocytes, possibly leading to decrease in catabolic activities of chondrocytes 29, 46. [score:8]
Having confirmed the role of IL-1β in miR-365 expression, we next examined the role of miR-365 expression on HIF-2α expression. [score:7]
In line with mRNA expression data (Fig.   2B), IL-1β -induced expression of HIF-2α was significantly suppressed by miR-365 transfection (Fig.   6A). [score:7]
However, miR-365 transfection significantly inhibited the basal expression of HIF-2α in IL-1β-untreated cells as well as IL-1β -induced HIF-2α expression (Fig.   2B). [score:7]
Downregulation of miR-365 resulted in the increased expression of HIF-2α and MMP-13 as well as a variety of other catabolic genes, including COX2, iNOS, and MMP-1, and -3, all of which are under the control of HIF-2α [9]. [score:6]
miR-365 was shown to significantly inhibit HIF-2α reporter activity relative to miR-con -treated cells, whereas transfection with anti-miR-365, the antisense inhibitor of miR-365, enhanced the reporter activity of HIF-2α 3′UTR (Fig.   4B, left). [score:5]
The suppression of miR-365 expression was not significantly different between 1 and 10 ng/mL of IL-1β except for at 16 h, when the decrease was only significant at 1 ng/mL concentration (Fig.   2A). [score:5]
In a recent report, miR-365 was up-regulated in OA chondrocytes compared to normal cells, while its level was suppressed in response to hydrostatic pressure [29]. [score:5]
Together, these data show that miR-365 suppresses HIF-2α expression by binding to the 3′UTR of HIF-2α mRNA. [score:5]
Figure 7Suppression of loss of ECM and expression of MMP-13 by miR-365 in the pellet culture. [score:5]
MAPK and NF-κB inhibitors had no significant influence on the basal expression of miR-365 and HIF-2α (Fig.   3B and C). [score:5]
MiR-365 downregulated HDAC4, resulting in decreased chondrocyte hypertrophy indicating that miR-365 is an important regulator of both chondrocyte hypertrophy and differentiation [28]. [score:5]
In this study, we examined whether miR-365 inhibits IL-1β-stimulated catabolic responses via modulation of HIF-2α expression in human chondrocytes. [score:5]
In addition, to examine the effect of HIF-2α knockdown on IL-1β-stimulated catabolic factor expression in miR-365-stimulated chondrocytes, si-HIF-2α and miR-365 were co -transfected into the chondrocytes. [score:4]
From this effort we identified has-microRNA-365 (miR-365), a miRNA previously implicated in ADAMTS-1 expression in breast cancer cell-line, as a potential regulator of HIF-2α. [score:4]
IL-1β treatment (1 and 10 ng/mL) significantly inhibited miR365 expression for 6, 16, 24, and 48 h compared to IL-1β-untreated cells (Fig.   2A). [score:4]
Furthermore, miR-365 transfection had no significant effect on COX-2 and iNOS as well as MMP-1, -3, and -13 expressions in the HIF-2α-knocked down chondrocytes (Fig.   6A–C). [score:4]
Recently, miR-365 was shown to be involved in chondrocyte differentiation through direct targeting histone deacetylase-4 (HDAC4) [28]. [score:4]
To examine the relationship between miR-365 and HIF-2α expression in OA progression, we compared the expression of miR-365 and HIF-2α in normal and OA cartilages. [score:4]
Additionally, miR-365 has been shown to affect two cartilage matrix regulation genes, including Runx1tl (runt-related transcription factor 1; translocation to, 1) expression in brown fat differentiation, and ACVR1/Alk-2, which encodes a bone morphogenetic protein (BMP) type I receptor 20– 27. [score:4]
The reporter activity data showed that a mutation in the miR-365 binding sequence removed miR-365 -mediated inhibition or anti-miR-365 -mediated enhancement of HIF-2α 3′UTR reporter activity (Fig.   4B, right). [score:4]
Therefore, these results demonstrate that both miR-365 and HIF-2α expression are regulated by IL-1β via MAPK and NF-κB. [score:4]
Human primary chondrocytes were transfected with miR-365 and miR-con 48 h prior to IL-1β stimulation for 6 h. IL-1β was observed to significantly reduce miR-365 expression and increase HIF-2α expression compared to IL-1β-untreated control (Fig.   2B). [score:4]
In contrast to our result, previous reports showed that miR-365 was up-regulated by IL-1β stimulation and in rat anterior cruciate ligament (ACL) surgery induced OA cartilage as well as human OA cartilage 29, 46. [score:4]
HIF-2α expression was attenuated by the direct binding of miR-365 to the 3′UTR of HIF-2α mRNA. [score:4]
Given the effects of IL-1β on miR-365 and HIF-2α expression, we examined the potential regulatory effects of miR-365 on IL-1β-activated signaling pathways. [score:4]
Bioinformatics analysis of IL-1β-regulated miRNAs using miRanda, TargetScan, and PicTar revealed a putative binding site for miR-365 in the 3′UTR of the catabolic transcription factor HIF-2α. [score:4]
Taken together, these results demonstrate that miR-365 regulates IL-1β -induced HIF-2α expression. [score:4]
Taken together, these data demonstrated that miR-365 significantly suppressed IL-1β -induced catabolic effects in 3D culture of primary chondrocytes. [score:3]
Figure 6Suppression of IL-1β -mediated catabolic effect by miR-365. [score:3]
Next, we sought to identify the IL-1β-activated signaling pathways that contribute to miR-365 and HIF-2α expression. [score:3]
However, miR-365 suppressed the reduction of pellet size induced by IL-1β, which significantly reduced the size of miR-con -transfected pellet (Fig.   7A). [score:3]
To examine the effect of MAPK and NF-κB signaling pathway on miR-365 and HIF-2α expression, chondrocytes were pretreated with SP600125 (10 µM), PD98059 (10 µM), SB203580 (1 µM), and Bay 11-7082 (5 µM) 2 h prior to stimulation with IL-1β (1 ng/mL) for 6 h. For isolation of total RNA from cartilage tissues, minced cartilage samples were ground to a fine powder in liquid nitrogen, and total RNA was isolated from chondrocytes using TRIzol reagent. [score:3]
Whether the regulation of HIF-2α by HDAC4 in chondrocytes is an upstream event of the catabolic regulation by miR-365 is a subject of further research. [score:3]
Our results prove that HIF-2α is a target of miR-365, suggesting that miR-365 plays a crucial role in maintaining cartilage homeostasis. [score:3]
Figure 4HIF-2α mRNA is a target of miR-365. [score:3]
In summary, we demonstrate that miR-365 levels were significantly suppressed in OA cartilage, and that IL-1β decreased the level of miR-365 in articular chondrocytes through activation of MAPK and NF-κB signaling pathways. [score:3]
Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) to detect the expression of HIF-2α and miR-365. [score:3]
The average age of cartilage donors (approximately 71 yrs vs 62.7 or 56.2 yrs), and control specimens classification (cartilage from the femoral head of patients with femur neck fracture and no known history of OA or RA vs cartilage (normal looking non -loaded area) from patient with primary or traumatic OA) might have caused the discrepancy in miR-365 expression in OA cartilage. [score:3]
Figure 1Relative expression of microRNA-365 (miR-365) and hypoxia-inducible factor-2 alpha (HIF-2α) in normal and osteoarthritic (OA) cartilage. [score:3]
However, our result showed that both at 1 and 10 ng/mL IL-1β decreased miR-365 expression which persisted throughout the experiment duration spanning from 1 to 48 hours. [score:3]
HIF-2α siRNA (si-HIF-2α; sense 5′-CGU-GAG-AAC-CUG-AGU-CUC-A-3′; antisense 5′-UGA-GAC-UCA-GGU-UCU-CAC-G-3′), control siRNA (si-con; sense 5′-CCU-ACG-CCA-CCA-AUU-UCG-U-3′; antisense 5′-ACG-AAA-UUG-GUG-GCG-UAG-G-3′) as a negative control, the mature form of has-miR-365 (miR-365; 5′-UAA-UGC-CCC-UAA-AAA-UCC-UUA-U-3′), and nonspecific microRNA (miR-con; 5′-CCU-ACG-CCA-CCA-AUU-UCG-3′) as a off-target control were purchased from Bioneer (Daejeon, Korea). [score:3]
Transfection with miR-365 significantly inhibited IL-1β -induced phosphorylation of ERK and p38 and IL-1β -induced translocation of p65 into the nucleus in human chondrocytes, while the phosphorylation of JNK was unaltered (Fig.   5A–D). [score:3]
The antisense inhibitor of miR-365 (anti-miR-365) was obtained from Applied Biosystems. [score:3]
Figure 3Modulation of miR-365 and HIF-2α expression by IL-1β signaling pathways. [score:3]
Primary chondrocytes were transfected with miR-con and miR-365 and stimulated with IL-1β (1 ng/mL) for 6 h. The level of miR-365 expression was quantified by qRT-PCR. [score:3]
Human OA chondrocytes were transfected with miR-365 or miR-con and si-con or si-HIF-2α for 48 h and stimulated with IL-1β (1 ng/mL) for 24 h. (A) Expression of HIF-2α, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in cell lysates and (C) matrix metalloproteinases (MMP-1 and -3) in the culture medium were analyzed by Western blot. [score:3]
These results suggest that miR-365 alleviates IL-1β -induced catabolism by modulating HIF-2α at the posttranscriptional level, and through cross-regulation of MAPK-NF-kB signaling. [score:2]
These results demonstrate that miR-365 functions as a regulator of IL-1β -induced pro-inflammatory and catabolic factors via modulation of HIF-2α. [score:2]
To confirm that miR-365 is regulated by IL-1β 17– 19, we investigated miR-365 expression in IL-1β -treated primary chondrocytes using qRT-PCR. [score:2]
MiR-365 and HIF-2α expression were related with IL-1β signaling pathways. [score:2]
To ensure that HIF-2α is the target of miR-365, we performed AGO2-RNP IP assay on miR-con- and miR-365 -transfected chondrocytes. [score:2]
As expected, the secreted MMP-13 levels in both IL-1β-untreated and IL-1β-stimulated pellet culture of primary chondrocytes and SW1353 cells were significantly suppressed by miR-365 transfection compared to the miR-con transfected groups (Fig.   7B). [score:2]
Altered expression of miR-365 and HIF-2α in OA compared to normal cartilage. [score:2]
HIF-2α was not detected in the HIF-2α-knocked down cells regardless of miR-365 transfection (Fig.   6A). [score:2]
Expression of mature miR-365 was quantified using a Taqman miRNA reverse transcription kit and miRNA-specific primers obtained from Applied Biosystems (Foster, CA, USA) according to the manufacturer’s instructions. [score:2]
Next, to confirm the association of miR-365 with HIF-2α 3′UTR, we examined the interaction of miR-365 or anti-miR-365 and a mutant reporter plasmid containing mutations in the miR-365 binding site of HIF-2α. [score:2]
MiR-365 and control microRNA (miR-con) were purchased from Bioneer (Daejeon, Korea). [score:1]
Human primary chondrocytes and SW1353 cells were transfected with miR-con or miR-365 and the pellets formed by centrifugation were stimulated with IL-1β (1 ng/mL) for 7 days. [score:1]
The 3′UTR sequence (5′-UGUUGCCCUGGCAUUAAGGGCAUUUUACCCUUGCAUUU-3′) of HIF-2α containing the putative miR-365 binding site were obtained from gene sequence databases, and used to design the wild-type HIF-2α 3′UTR-Luc plasmid (HIF-2α 3′UTR). [score:1]
In addition, alcian blue staining for ECM showed that IL-1β caused fragile cell masses and weak staining in miR-con -transfected group, whereas miR-365 significantly prevented IL-1β -induced changes in cell mass and ECM matrix (Fig.   7A). [score:1]
MiR-365 expression was significantly reduced in OA compared to normal cartilages (Fig.   1A), while HIF-2α mRNA level was increased in OA cartilage relative to controls (Fig.   1B). [score:1]
miR-365 prevented IL-1β -induced MMP-13 and loss of extracellular matrix (ECM) in pellet culture of chondrocytes. [score:1]
Our luciferase assay confirmed that miR-365 directly interacts with the 3′UTR of HIF-2α mRNA. [score:1]
Human OA chondrocytes were transfected with miR-365 or a nonspecific control miRNA (miR-con) for 48 h and stimulated with IL-1β (1 ng/mL) for 0, 15, 30, and 60 min. [score:1]
It has been reported that miR-365 plays a role in a variety of cellular processes including cell proliferation, apoptosis, and differentiation. [score:1]
Primary chondrocytes and SW1353 cells were incubated with miR-365 or miR-con (50 nM) diluted in Lipofectamine for 2 h. The pellets of miR-365- or miR-con -transfected cells were formed by centrifugation 4 × 10 [6] cells at 500 g for 10 min and transferred into bottom round 96-well plate. [score:1]
Figure 5Effect of miR-365 on IL-1β-activated signaling pathways in human chondrocytes. [score:1]
To investigate whether miR-365 suppresses loss of ECM induced by IL-1β, the pellet culture of miR-365 -transfected chondrocytes was performed in DMEM containing IL-1β for 7 days. [score:1]
miR-365 -transfected cells. [score:1]
Human chondrocytes were transfected with miR-con, miR-365, or anti-miR-365 at a concentration of 50 nM using Lipofectamine according to the manufacturer’s instructions. [score:1]
Briefly, si-HIF-2α and/or miR-365 were prepared by gently pipetting in Lipofectamine reagent diluted with Opti-MEM media. [score:1]
Using an unbiased bioinformatics analysis of IL-1β-stimulated miRNAs, we identified a putative binding site for miR-365 in the 3′UTR of the catabolic transcription factor HIF-2α. [score:1]
The pellet morphology data demonstrated that no significant changes were observed in the size of miR-con- and miR-365 -transfected primary chondrocyte and SW1353 cell pellets in the absence of IL-1β (Fig.   7A). [score:1]
To address this question, primary chondrocytes were transfected with miR-365 and miR-con for 48 h followed by stimulation with IL-1β (1 ng/mL) for 15–60 min. [score:1]
To confirm whether the silencing of HIF-2α counteracts miR-365 -induced reduction of procatabolic effects stimulated by IL-1β, chondrocytes were transfected with si-HIF-2α and miR-365. [score:1]
MiR-365 was shown to confer anti-tumor activity in multiple human cancer cell lines by means of cell cycle regulation and induction of apoptosis 41– 43. [score:1]
IL-1β + miR-365 -transfected cells. [score:1]
IL-1β-stimulated catabolic factors were reduced by miR-365 in chondrocytes. [score:1]
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2.4. miR-365 Directly Targets HDAC4 Leading to Down-Regulation of HDAC4 Expression. [score:9]
We examined the mRNA level of hypertrophic marker gene Col X. Indeed, overexpression of miR-365 significantly up-regulated Col X and further increase of IL-1β induced the up-regulation of Col X (Figure 2C). [score:9]
The up-regulation of miR-365 further contributes to cartilage catabolic effects in OA through inhibition of its target HDAC4. [score:8]
Although the critical role of miR-365 in cartilage maintenance may be explained largely by identifying HDAC4 as its direct target, miRNAs are believed to regulate multiple target mRNAs. [score:7]
Understanding the regulation of miR-365 in this pathophysiological condition is of great importance and could open up new therapeutic avenues targeting the disease. [score:6]
miR-365 overexpression and IL-1β treatment have a synergistic effect on the down-regulation of HDAC4 (Figure 6B). [score:6]
To investigate whether the expression of miR-365 was induced by IL-1β, primary human chondrocytes were stimulated with IL-1β for 24 h. IL-1β stimulation of chondrocytes resulted in significant up-regulation of miR-365 expression (Figure 2A). [score:6]
More interestingly, IL-1β significantly reduced expression of HDAC4 mRNA, which resembled the effect of miR-365 overexpressing chondrocytes (Figure 6B). [score:5]
Primary cultured human chondrocytes were serum starved overnight and then treated with 10 ng/mL recombinant human IL-1β (Roche, Branchburg, NJ, USA) for 24 h. Human miR-365 mimic, miR-365 inhibitor and their negative control mimics or inhibitors were obtained from Dharmacon (Thermofisher Scientific). [score:5]
Western blotting results further confirmed the inhibition of HDAC4 mRNA and protein expression by miR-365 while anti–miR-365 enhanced the mRNA and protein level of HDAC4 in human chondrocytes (Figure 5B,C). [score:5]
The expression of miR-365 was significantly up-regulated by cyclic loading compared with its non-load control (Figure 1A). [score:5]
Xu Z. Xiao S. B. Xu P. Xie Q. Cao L. Wang D. Luo R. Zhong Y. Chen H. C. Fang L. R. miR-365, a novel negative regulator of interleukin-6 gene expression, is cooperatively regulated by Sp1 and NF-κB J. Biol. [score:5]
Inhibition of miR-365 or Overexpression of HDAC4 Impairs IL-1β Induction of MMP13 mRNA. [score:5]
Manipulation of the expression of miR-365 in articular chondrocytes by a miR-365 inhibitor may be a potent therapeutic for the prevention and treatment of OA. [score:5]
The expression of miR-365 was significantly up-regulated in OA cartilage compared with normal cartilage (Figure 3D). [score:5]
To further clarify the molecular mechanism underlying miR-365 on OA pathogenesis, we are interested in identifying the direct target of miR-365 that may be involved in OA development. [score:5]
Furthermore, inhibition of miR-365 reduced the IL-1β induced catabolic effect as shown by significant inhibition of MMP13 (Figure 6C). [score:5]
2.2. miR-365 is Up-Regulated by Pro-inflammatory Cytokine IL-1β and is Essential for Cartilage Degeneration. [score:4]
To further determine whether miR-365 is up-regulated in OA cartilage in vivo, we used the surgical arthritis mo del to experimentally induce OA pathogenesis, in which the articular cartilage was exposed to an excessive mechanical load, due to joint instability caused by surgical resection of the anterior cruciate ligament (ACL) in rats. [score:4]
We further show HDAC4 is a direct target of miR-365, which mediates mechanical stress and inflammation in OA pathogenesis, thereby leading to accelerated cartilage destruction. [score:4]
This is consistent with our study that cyclic loading and IL-1 both up-regulate the transcription of miR-365 through activation of NF-κB. [score:4]
To identify whether HDAC4 is a direct target of miR-365 in human chondrocytes, we transfected a wild-type HDAC4 3′-UTR construct containing a putative miR-365 binding sequence. [score:4]
HDAC4 protein expression is modulated by miR-365, and this regulatory effect is driven by the miR-365 conserved seed sites within the 3′-UTR of HDAC4. [score:4]
In this study, we showed that HDAC4 is a direct target of miR-365 in human articular chondrocytes at different levels. [score:4]
Furthermore, we found that the construct bearing mutations at a putative miR-365 binding site completely abolished the inhibitory effect of miR-365 (Figure 5A). [score:4]
We therefore asked whether miR-365 is sufficient to up-regulate metallopeptidase 13 (MMP13), a crucial effector of OA cartilage destruction. [score:4]
Therefore, cyclic loading transcriptionally up-regulates miR-365 through NF-κB signaling. [score:4]
In vivo work using transgenic animal mo dels to overexpress miR-365 or knockout miR-365 in cartilage will be needed to establish the definite etiologic answer for miR-365 in OA pathogenesis. [score:4]
We have identified that mechanical loading up-regulated miR-365 in growth plate chondrocytes. [score:4]
MMP13 was significantly up-regulated by transfection of chondrocytes with miR-365 mimic and was exacerbated by IL-1β treatment (Figure 2D). [score:4]
A Luciferase reporter assay revealed that overexpression of miR-365 significantly inhibited reporter activity in human chondrocytes. [score:4]
Furthermore, miR-365 is transcriptionally up-regulated by cyclic loading and IL-1β stimulation through the activation of NF-κB signaling in the articular chondrocytes. [score:4]
This further supports the notion that HDAC4 may be a direct target of miR365, which mediates OA pathogenesis. [score:4]
Taken together, these findings suggest that miR-365 directly targets HDAC4 in human chondrocytes and mediates its catabolic effects. [score:4]
Cyclic Loading Transcriptionally Up-Regulates miR-365 through NF-кB Signaling. [score:4]
To further confirm that miR-365 contributes to OA pathogenesis through HDAC4, we examined the expression of HDAC4 in human OA cartilage. [score:3]
Therefore, miR-365 contributes to OA pathogenesis by targeting HDAC4 through two mechanisms: hypertrophic conversion of articular chondrocytes through RUNX2 and MEF2C (Figure 5C) and promoting inflammatory cytokine production to increase catabolic effects. [score:3]
We found that cyclic loading in 3D chondrocytes and disruption of extracellular matrix (ECM) by mechanical instability induced by anterior cruciate ligament transection (ACLT) surgery, triggered increased miR-365 expression in cartilage. [score:3]
To further confirm relations between OA and miR-365 in human cartilage, we quantify the miR-365 expression level in primary OA (PA) and traumatic OA (TA) groups, which were divided according to the patient’s medical history. [score:3]
In conclusion, our results collectively indicate that miR-365 acts as a mechanically induced mediator of osteoarthritic cartilage destruction, by directly regulating HDAC4. [score:3]
We have found a significant difference in miR-365 expression in the OA vs. [score:3]
The miR-365 expression levels in the lesion area were significantly higher than the corresponding non-lesion control area in both the primary OA and traumatic OA groups (Figure 4A,B). [score:3]
We have shown that miR-365 is expressed at a higher level in OA cartilage (Figure 4B,C). [score:3]
2.3. miR-365 Expression Is Increased in Osteoarthritis (OA) Cartilage. [score:3]
In this study, we observed mechanical responsive miR-365 is expressed at higher levels in both primary OA and traumatic OA cartilage. [score:3]
Overexpression of miR-365 induces chondrocyte differentiation marker Ihh and MMP13 and exacerbates the IL-1 induced catabolic effects in chondrocytes. [score:3]
miR-365 is expressed at higher levels in human OA cartilage from primary OA patients as well as OA patients with traumatic history, supporting its pathological significance. [score:3]
Total protein was extracted from human articular chondrocytes 48 h post-transfection of miR-365 mimic or inhibitor and their controls. [score:3]
The expression of miR-365 in OA chondrocytes was significantly higher than that in the relative normal chondrocytes (Figure 3A). [score:3]
In this study, we explain a possible causal relationship between the mechanical stress and pro-inflammatory stimuli responsive miR-365, which regulates catabolic effects in human articular chondrocytes and mediates OA development. [score:3]
It remains unknown whether this involves regulation of miR-365 or other mechanical sensitive miRNAs. [score:2]
Therefore, the role of miR-365 in cartilage homeostasis may involve the regulation of additional genes. [score:2]
pGL-HDAC4-mut was derived from pGL-HDAC4 by mutating 3 bases pairs within miR-365 seed sites within the HDAC4 3′-UTR sequence using the QuikChange XL Site-directed Mutagenesis kit (Stratagene, La Jolla, CA, USA). [score:2]
Cyclic loading is sufficient for the transcriptional regulation of miR-365 through NF-κB signaling. [score:2]
As a result, the downstream Runx2 and MEF2C were regulated by miR-365 and contribute to hypertrophic conversion of chondrocytes in OA cartilage. [score:2]
To determine whether miR-365 is involved in OA pathogenesis, we compared its expression level between normal and OA chondrocytes. [score:2]
However, we failed to conclude that traumatic OA cartilage expresses higher levels of miR-365 compared with primary OA cartilage. [score:2]
miR-365 expression level was quantified with the Taqman microRNA assays specific for mature miR-365 (Life Technologies). [score:2]
Furthermore, in the late stage of OA, stress from the combination of overload and inflammatory cytokines further increases miR-365, leading to cartilage degradation. [score:1]
However, our data demonstrate miR-365 is induced by mechanical stress as well as an inflammatory cytokine which contributes to the pathological sequence of OA progression. [score:1]
We aim to address the role of mechanical sensitive miR-365 in OA by using human articular chondrocytes, an animal mo del and osteoarthritis patients and traumatic osteoarthritis patients. [score:1]
Here, we identify that miR-365 is a mechanically induced mediator of cartilage degeneration. [score:1]
The luciferase reporter plasmid TSS-1348, TSS-1097, TSS-705, and TSS-336, which contains the 1348-, 1097-, 705-, and 336-bp proximal promoter sequences upstream of TSS of miR-365, respectively, were a generous gift from Professor Liu-Rong Fang from Hua-Zhong agriculture University, Wuhan, China [24]. [score:1]
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In all cases, downregulating the targets of a given miRNA rescued differentiation upon inhibition of this miRNA, but did not do so when a different miRNA was inhibited: for example, downregulating miR-365 targets (PIK3R3, MAPK1, XPO4 and CNOT6L) rescued inhibition by miR-365 LNA but not by miR-1249 or miR-486-5p LNAs. [score:17]
In particular, downregulating the miR-365 target CNOT6L restored cell fusion and MCK expression, but not MHC expression (Figure 4c et S3e). [score:10]
CNOT6L, XPO4 were regulated by miR-365 overexpression or downregulation (Figure 4e), and could be validated as direct targets, either by a assay [14] in which mRNA targets are biochemically pulled down (Figure 4f) or, when this assay was not sensitive enough, by a standard reporter assay (Figure 4g). [score:9]
Let-7 family LNAs are specific of the let-7 family (there is no significant inhibition of miR-365), and also more efficient on the targeted isoforms, even though each LNA also inhibits the other isoform. [score:7]
Some of these hit target proteins have been previously characterized as inhibitors of myotube differentiation: the miR-486-5p target FOXO1 [21] and the miR-365 target ERK2 [22]. [score:7]
These data indicate that distinct pathways, leading to MHC expression, cell fusion and/or MCK expression are all under the control of miR-365. [score:5]
In contrast, downregulating XPO4 (or PIK3R3), which are also targets of miR-365, restored all measured parameters. [score:4]
The miR-365 target PIK3R3 binds the IGFR1 receptor and is involved in regulating cell proliferation by the IGF cytokines [24]. [score:4]
The miR-365 target ZNF148 (ZBP-89) is a zinc finger protein that was shown to regulate multiple promoters in myoblast cells [23]. [score:4]
This selection of hits included two pro-differentiation miRNAs, miR-1249 and miR-365; one anti-differentiation miRNA, miR-98; and a miRNA required for myoblast survival, miR-361-3p – note that miR-98 and miR-365 have similar expression profiles but have opposite effects on differentiation. [score:3]
C2C12 mouse myoblast cells stably transduced with a vector expressing a tagged version of AGO2 were transfected with biotinylated miR-365, or miR-20a as a control, and extracts were submitted to tandem affinity purification followed by detection of associated mRNAs by RT-QPCR (MAP: MAPK1; XP: XPO4; STAT: STAT3). [score:3]
html) for four hit miRNAs: miR-486-5p, miR-361, miR-365 and miR-1249 (list of the targets tested in Figure S3d). [score:3]
The specificity of phenotypic rescue was first confirmed for miR-365, using siRNAs against putative targets of this and other miRNAs, by monitoring differentiation markers using immunofluorescence (Figure 4c) and western blot (Figure S3e). [score:3]
C2C12 mouse myoblastic cells stably transduced with a vector expressing a tagged version of AGO2, or with the empty vehicle vector for the control, were transfected with biotinylated miR-365, or miR-20a as a control. [score:3]
A pSiCheck reporter vector (Promega) containing 3.230 kb of either CNOT6L 3′UTR wild-type (nt 2710 to 5940) or mutant (the miR-365 seeds, gggcatt, were mutated into gtgcagt using the AccuPrime Pfx site-directed mutagenesis system - Life Technology) was transfected into C2C12 cells (a murine myoblast cell line), along with a control miRNA precursor or miR-365 precursor (50 nM final concentration). [score:2]
Mir-365 appears to be highly expressed in LHCN cells (as judged from RT-QPCR results, Figure S2c) and might thus be in excess in the cells. [score:2]
Only one mimic out of six, miR-365, had no effect on differentiation (Figure S2b). [score:1]
LHCN cells were treated with miR-365 LNA or mimic as indicated, and CNOT6L and XPO4 proteins were detected by western blotting 48 h later. [score:1]
LHCN cells were transfected with miR-365 LNA along with indicated siRNAs (2 siRNAs per gene), and extracts were analyzed at day 7 by western blot with indicated antibodies; cont: control; CNO: CNOT6L; PI3: PIK3R3 MAP: MAPK1; XPO: XPO4. [score:1]
79 ** hsa-mir-365 7.13 *** 77.53 *** hsa-mir-429 54.63 *** 85.25 *** hsa-mir-454 33.25 *** 87.31 - hsa-mir-455-3p 42.76 *** 96.4 - hsa-mir-484 4.83 *** 78.73 - hsa-mir-485-3p 4.75 *** 71.49 *** hsa-mir-501-3p 69.25 *** 91.25 *** hsa-mir-512-5p 21.37 *** 72.89 *** hsa-mir-532-3p 9.5 *** 85.93 *** hsa-mir-541 69.87 *** 97.77 - hsa-mir-600 35.63 *** 93.48 - hsa-mir-625* 28.5 *** 72.89 *** Hits of functional screen Relative percentage of myotubes 1, % of control p value, Mann Whitney test Relative cell count 2, % of control p value, Mann Whitney test hsa-mir-636 2.37 *** 81.98 *** hsa-mir-663 21.38 *** 84.73 *** hsa-mir-664 7.13 *** 82.85 *** hsa-mir-766 45.13 *** 73. [score:1]
Extracts were submitted to tandem affinity purification, first with anti-Flag antibodies (to immunoprecipitate AGO complexes) and then with streptavidin (to purify miR-365 complexes). [score:1]
ctrl: control; 365: miR-365. [score:1]
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[+] score: 67
MiR-365a expression is upregulated in breast tumors and is a potential circulating marker for estrogen receptor -positive breast tumors. [score:5]
Experimental analysis of changes in mRNA expression demonstrated that overexpression of miR-365a in MDA-MB-231 and S KOV3. [score:5]
Half of the mice were treated with a control miRNA hairpin inhibitor and the other half were treated with the miR-365a hairpin inhibitor. [score:5]
The effect of miR-365a upregulation may be context specific as demonstrated by the opposite association with survival in uterine cancer patients and differential association with survival in breast cancer subtypes. [score:4]
15, 17, 18, 29 Our analysis demonstrated that miR-365 exerts pleiotropic effects by targeting multiple gene transcripts including regulatory genes, such as chromatin modifiers. [score:4]
In particular we studied miR-365a whose expression is associated with poor survival across several cancer types and demonstrated that anti-miR-365 significantly reduced tumor formation in animal mo dels. [score:3]
Expression of miR-365a in several cancer types in The Cancer Genome Atlas data was markedly associated with poor patient survival (Figure 6e). [score:3]
We thus examined the functional consequences of miR-365a expression on the growth of tumor cells in vivo. [score:3]
Further analysis of one such miRNA, mir-365a, identified its role in regulating epigenetic modification of chromatin and its dysregulation in multiple cancers. [score:3]
Multiple pathways in our screen were affected by expression miR-365a (Figure 5). [score:3]
We performed a survival analysis to determine whether miR-365a expression is associated with cancer patient clinical outcomes. [score:3]
We demonstrated that targeting miR-365a with anti-miR-365 resulted in significant reduction of tumors in a xenograft mo del. [score:3]
Given the observed pleiotropic effect of miR-365a, we performed gene ontology -based analysis of targets of miR-365a that are bound by argonaute in argonaute cross-linked immunoprecipitation and next-generation sequencing (AGO-CLIP-seq) cell line experiments [21] and found a strong association with chromatin modification pathways (Figure 6a,b). [score:3]
[15] Previous studies demonstrated that miR-365a targets BCL2 and cyclin D, 16, 17 NKX2-1, 18, 19 and HDAC4. [score:3]
MiR-365a regulates many pathways besides the cell cycle owing to its high level regulation of genes via regulation of chromatin modifiers. [score:3]
We found that miR-365 functionally regulated the most proteins in steroid hormone, EMT, cell cycle, PI3K/AKT and MAPK pathways. [score:2]
Interestingly, the clustering of miR-365a with other cluster 2 miRNA is likely due to its regulation of cell cycle proteins. [score:2]
We identified miR-365, miR-555 and miR-665 as important regulators of multiple cellular pathways—miR-365 being previously implicated in cancer pathophysiology. [score:2]
[20] In the present study, we found that miR-365a functional regulated steroid hormone, EMT, cell cycle, PI3K/AKT, and MAPK pathways. [score:2]
MiR-365a regulates chromatin modifiers. [score:1]
ip1 tumor-bearing mice resulted in marked reductions in tumor weight and nodule number (Figure 6f), which is consistent with miR-365a having a major role in tumor progression. [score:1]
Previous studies and our present results demonstrated miR-365a involvement in numerous critical functional pathways underscored the importance of this miRNA in cancer. [score:1]
Treatment with miR-365a antimir (anti-miR-365a) incorporated in dioleoylphosphatidylcholine nanoliposomes of S KOV3. [score:1]
Gene expression measurements of miR-365a -treated S KOV3. [score:1]
ip1 cells is not decreased by miR-365a in 2D cultures (Supplementary Figure 8), unlike the majority other cluster 2 miRNAs. [score:1]
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5
[+] score: 55
At basal conditions we observed that the expression levels of miR-27a, miR-140, and miR-146a were significantly downregulated in OA cell cultures in comparison to normal (p < 0.01), while miR-365 was upregulated in OA chondrocytes (p < 0.01). [score:9]
miR-365 is also correlated with cartilage catabolic processes in OA: its upregulation in OA chondrocyte cultures is induced by mechanical overloading, through the inhibition of its target gene histone deacetylase (HDAC)-4. Furthermore, miR-365 is a mediator of inflammatory response [23]. [score:8]
Yang X. Guan Y. Tian S. Wang Y. Sun K. Chen Q. Mechanical and IL-1β responsive miR-365 contributes to osteoarthritis development by targeting histone deacetylase 4 Int. [score:4]
Following in vitro transfection studies, HDAC-4 was identified as a direct target gene of miR-365 [23]. [score:4]
The upregulation of miR-365 contributed to an abnormally accelerated differentiation and proliferation of hypertrophic chondrocytes and inflammatory cytokine production, increasing catabolic effects [23]. [score:4]
The aim of this study was to evaluate if a cyclic HP could influence cell transcriptional activity, modifying miR-27a/b, miR-140, miR-146a/b, and miR-365 expression levels, which are responsible for the regulation of mRNA levels of their target genes, MMP-13, ADAMTS-5, IGFBP-5, and HDAC-4, in normal and OA chondrocyte cultures. [score:4]
In addition, Yang et al. observed that miR-365 was upregulated by an injuring mechanical loading, and by the stimulation with pro-inflammatory cytokines [23]. [score:4]
Since the responsiveness of miR-365 at mechanical loading, the HDAC-4 expression levels modulation after pressurization was expected. [score:3]
Our evidence highlighted the beneficial role of HP suggesting the involvement of other factors activated by loading, different by miR-365, in the regulation of transcriptional activation of HDAC-4. The canonical Wnt signaling pathway plays a fundamental role in embryonic skeletal development and articular cartilage growth and homeostasis [46, 47, 48]. [score:3]
Following HP used in our study at all the analyzed time points, miR-365 gene expression was significantly reduced in OA cultures. [score:3]
The purpose of this study was to investigate the possible effect of cyclic hydrostatic pressure (HP) (1–5 MPa, 0.25 Hz) on miR-27a/b, miR-140, miR-146a/b, and miR-365 expression levels, as well as on the mRNA levels of their target genes, MMP-13, ADAMTS-5, IGFBP-5, and HDAC-4, in human normal and OA chondrocyte cultures. [score:3]
reported that miR-365 regulated the protein levels of HDAC-4, but not its mRNA levels [45]. [score:2]
The present study confirms previous data reported by Yang et al. showing the overexpression of miR-365 in OA chondrocyte cultures compared to normal cells. [score:2]
The observed reduction of miR-365 after HP, should be associated by an increase of HDAC-4 mRNA. [score:1]
Concerning miR-365, our data showed its significant reduction after pressurization at the different analyzed time points in OA cells (p < 0.01). [score:1]
[1 to 20 of 15 sentences]
6
[+] score: 37
In lung cancer, down-regulation of miR-365 has been implicated in increased expression of thyroid transcription factor 1 (TTf1), important for lung development and commonly up-regulated in lung tumors [32]. [score:10]
Conversely, in colon cancer, up-regulation of miR-365 is thought to repress tumor formation and maintenance by targeting the anti-apoptotic genes BCL-2 and cyclin D1. [score:6]
Conformational studies revealed, however, that only miR-365, miR-193b,, and were expressed in the lymphoblast cell line; and only showed a significant change in expression in response to NRF2 activation. [score:5]
Downregulated miR-365 in colon cancer increases sensitivity to 5-fluorouracil [33]. [score:4]
miRNA Location Targets References miR 193b/365Chr16,14397824-14397906 (miR193b)14403142-14403228 (miR-365)TTf1 - oncogenicBCL2 – TSGCyclin D- TSG, uPa(Qi et al., 2012)(Nie et al., 2012)(Li et al., 2009) Chr7, 130562218-130562298Sp-1MCL-1 - oncogenicTCL1 – oncogenic(Amodio et al., 2012)(Mott et al., 2007)(Pekarsky et al., 2006) Chr19, 13985513-13985622SIRT1- oncogenic and TSGKRAS - oncogenicTGFβ - TSGTNF - TSGNOTCH - oncogenic and TSG(Zhang et al., 2012)(Schonrock et al., 2012)(Hashimoto et al., 2010) miR-617 Chr12, 81226312-81226408 N/A miR-592 Chr7, 126698142-126698238 N/A miR-1207 Chr8 129061398-129061484. [score:3]
HBEGF (Papagregoriou et al., 2012) Chr9- 111808509-111808578PIK3IP1 - TSGBTG2 – TSG (Jalava et al., 2012) Chr12, 7072862-7072929ZEB1, FHOD1, PPM1F,TUBB3-TBK1, BMI1-oncogenicPPP2R1B - TSG(Burk et al., 2008)(Jurmeister et al., 2012)(Cochrane et al., 2010)(Lin et al., 2012) miR-550 Chr7, 30329410-30329506 CPEB4 (Tian et al., 2012) Aberrant expression of the miR-365/193b cluster has been linked to malignancies such as MM, lung cancer, and colon cancer. [score:3]
Aberrant expression of the miR-365/193b cluster has been linked to malignancies such as MM, lung cancer, and colon cancer. [score:3]
Finally ChIP-Seq data indicates that NRF2 can regulate the miR-365/193b cluster [20]. [score:2]
Interestingly, both miR-365 and miR-193b can be tumor associated without the other member of the cluster. [score:1]
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7
[+] score: 29
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]
Similar results were obtained when co -expressing miR-365 with c-Myc or AKT/Ras (Supplementary Figure 7A–7D). [score:3]
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8
[+] score: 27
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-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-31, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-181a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-184, hsa-mir-186, hsa-mir-193a, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-219a-2, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-365b, hsa-mir-374a, hsa-mir-148b, hsa-mir-423, hsa-mir-486-1, hsa-mir-499a, hsa-mir-532, hsa-mir-590, bta-mir-26a-2, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-221, bta-mir-222, bta-mir-27a, bta-mir-499, bta-mir-125b-1, bta-mir-181a-2, bta-mir-205, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-193a, bta-let-7d, bta-mir-148b, bta-mir-186, bta-mir-191, bta-mir-192, bta-mir-200a, bta-mir-214, bta-mir-22, bta-mir-23a, bta-mir-29c, bta-mir-423, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-mir-532, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-365-1, bta-mir-374a, bta-mir-99b, hsa-mir-374b, hsa-mir-664a, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-1915, bta-mir-146a, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-194-2, bta-mir-219-1, bta-mir-223, bta-mir-26a-1, bta-mir-365-2, bta-mir-374b, bta-mir-486, bta-mir-763, bta-mir-9-1, bta-mir-9-2, bta-mir-181a-1, bta-mir-2284i, bta-mir-2284s, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2339, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-664a, bta-mir-2284e, bta-mir-1388, bta-mir-194-1, bta-mir-193a-2, bta-mir-2284w, bta-mir-2284x, bta-mir-148c, hsa-mir-374c, hsa-mir-219b, hsa-mir-499b, hsa-mir-664b, bta-mir-2284y-1, bta-mir-2284y-2, bta-mir-2284y-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2284y-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2284z-4, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2284z-2, hsa-mir-486-2, hsa-mir-6516, bta-mir-2284ab, bta-mir-664b, bta-mir-6516, bta-mir-219-2, bta-mir-2284ac, bta-mir-219b, bta-mir-374c, bta-mir-148d
Within 6 hrs of the presence of E. coli, the expression of 6 miRNAs in MAC-T cells was significantly altered (P < 0.05), three were down regulated (bta-miR-193a-3p, miR-30c and miR-30b-5p) while three were up-regulated (bta-miR-365-3p, miR-184 and miR-24-3p) (Table  3). [score:7]
For example, gene targets of five differentially expressed miRNAs (miR-365-3p, miR-30b-5p, miR-30c, let-7a-5p and miR-23a) were enriched for pathways in immune system (B-cell receptor signaling pathway, chemokine signaling, T-cell receptor signaling and Fc gamma R -mediated phagocytosis). [score:5]
The three miRNAs (bta-miR-193a-3p, miR-30c and miR-30b-5p) that were significantly down regulated or one miRNA (bta-miR-365-3p) that was significantly up regulated within 6 hrs of E. coli presence only showed a retarded significant down regulation by 24 or 48 hrs (bta-miR-193a-3p, 30c and 30b-5p) or up regulation (bta-miR-365-3p) by 48 hrs in the presence of S. aureus. [score:5]
The expression of bta-miR-21-3p, miR-365-3p, miR-193a-3p, miR-423-5p and miR-486 in challenged cells was further confirmed by qPCR. [score:3]
For example, bta- miR-193a-3p and miR-365-3p for E. coli at 6 h, miR-21-3p and miR-423-5p for E. coli at 12 h, miR-423-5p for E. coli at 24 h, miR-193a-3p for E. coli at 48 h, miR-21-3p for S. aureus at 24 h, and miR-193a-3p and miR-365-3p for S. aureus at 48 h were similarly differentially expressed (P < 0.05) with both methods. [score:3]
Five differentially expressed miRNAs (bta-miR-193a-3p, miR-423-5p, miR-21-3p, miR-365-3p and miR-486) were validated by quantitative RT-PCR using TaqMan [®] miRNA Assays following manufacturer’s recommendations (Applied Biosystems, Foster City, CA, USA). [score:2]
010 bta-miR-21-3p2.1540.276 0.0171.0620.2720.819 bta-miR-365-3p0.9300.1150.5680.9940.1060.962 bta-miR-423-5p0.6290.046 0.0040.8120.1060.111 bta-miR-4861.6140.168 0.0321.6300.3420.14224hbta-miR-193a-3p1.2060.0520.0171.3270.1710.140 bta-miR-21-3p1.9420. [score:1]
4100.0921.2220.066 0.040 bta-miR-365-3p1.0510.3580.8790.8900.0960.478 bta-miR-423-5p1.8380.252 0.0461.3040.2970.336 bta-miR-4861.0990.0300.5450.8670.1190.48048hbta-miR-193a-3p0.3530.053 0.0200.3360.026 0.021 bta-miR-21-3p1.0830.1920.6791. [score:1]
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9
[+] score: 26
7 miRNAs (hsa-miR-144,hsa-miR-133a,hsa-miR-365, hsa-miR-424,hsa-miR-500, hsa-miR-661,hsa-miR-892b) had different gene expression levels between active TB and healthy controls; 4 of them (hsa-miR-144,hsa-miR-365 and hsa-miR-133a, hsa-miR-424) were up-regulated and 3 of them (hsa-miR-500, hsa-miR-661,hsa-miR-892b) were down-regulated in active TB patients. [score:9]
Interestingly, 5 of the miRNAs (hsa-miR-365, hsa-miR-223 and hsa-miR-144, hsa-miR-451, hsa-miR-424) were highly expressed in PBMCs and their expression in 3 groups was confirmed by qPCR. [score:5]
We analyzed the expression of 7 miRNAs (hsa-miR-223, hsa-miR-365 hsa-miR-424, and hsa-miR-451, hsa-miR-144, hsa-miR-500 and hsa-miR-21*) selected from the microarray data by qPCR. [score:3]
This difference between active and non-active TB groups was mainly due to the induced expression of hsa-miR-365, hsa-miR-223 and hsa-miR-302a, hsa-miR-486-5p, hsa-miR-144 and hsa-miR-451, hsa-miR-21* and hsa-miR-424 in active TB patients. [score:3]
We observed that hsa-miR-424 and hsa-miR-365 also exhibited increased expression levels in samples from active TB versus healthy control groups (P<0.05). [score:3]
The expression profiles of the active TB and LTBI groups were statistically different for miRNAs from group 1: hsa-miR-144 (P<0.05), hsa-miR-424 (P<0.01), hsa-miR-451(P<0.05), hsa-miR-223 (P<0.05), and hsa-miR-365 (P<0.05). [score:3]
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[+] score: 20
The mir-365 up-regulation was associated to the inflammation pathway [34], [35]. [score:4]
In situ hybridization probesLocked nucleic acid (LNA) hybridization probes complementary to human mature miR-let7b (5′-ACCACACAACCTACTACCTC-3′), miR-365 (5′-AGGATTTTTAGGGGCATT-3′), and to precursor of miR let7b (5′-TATCTTCCGAGGGGCAACA-3′), precursor of miR 302a (5′-GAAGCACTTACTTCTTTAGTTTC-3′) were provided from Exiqon (Vedbaek, Denmark). [score:1]
Hoechst 33342 staining of nuclei (lane 1), specific signal of scramble miRNA (A; negative control), U6 small nuclear RNA (B; positive control), let-7b (C), mir-365 (D), pre-let-7b (E) and pre-mir-302a (F) probes (lane 2) and MitoTracker® Red CM-H [2]XRos staining of respiring mitochondria (lane 3) are represented in gray scale. [score:1]
0020220.g004 Figure 4 Using 2.5 pmol of locked nucleic acid (LNA) probes prelabelled with digoxigenin, we determined in situ hybridization patterns of scramble miR (A; negative control), U6 small nuclear RNA (B; positive control), let-7b (C), mir-365 (D), pre-let-7b (E) and pre-mir-302a (F) probes (lane 1). [score:1]
In situ signal of mir-365, pre-mir-let7b and pre-mir-302a co-localized with functioning mitochondria in human myoblasts observed in confocal microscopy. [score:1]
Using 2.5 pmol of locked nucleic acid (LNA) probes prelabelled with digoxigenin, we determined in situ hybridization patterns of scramble miR (A; negative control), U6 small nuclear RNA (B; positive control), let-7b (C), mir-365 (D), pre-let-7b (E) and pre-mir-302a (F) probes (lane 1). [score:1]
The in situ hybridization clearly localized two pre-microRNA (pre-mir302a and pre-let-7b) and one microRNA (mir-365) in the mitochondria. [score:1]
In situ hybridization of pre-mir-302a, pre-let-7b and mir-365, using specific labelled locked nucleic acids and confocal microscopy, demonstrated that these miRNA were localized in mitochondria of human myoblasts. [score:1]
0020220.g005 Figure 5Using locked nucleic acid (LNA) probes, we performed in situ hybridization to localized mir-365, mir-let-7b, pre-let-7b and pre-mir-302a within the cell. [score:1]
As it circumvents the need for mitochondrial purification, this approach helped to clearly establish the localization of at least two pre-miRNA (prem-mir-302a and pre-let-7b) and one miRNA (mir-365) in human mitochondria. [score:1]
Mir-365, pre-mir-302a and pre-let7b specific fluorescent LNA were clearly co-localized in perinuclear mitochondria, as demonstrated by the yellow signal one could observed in that area (Figure 3D, E, F). [score:1]
Locked nucleic acid (LNA) hybridization probes complementary to human mature miR-let7b (5′-ACCACACAACCTACTACCTC-3′), miR-365 (5′-AGGATTTTTAGGGGCATT-3′), and to precursor of miR let7b (5′-TATCTTCCGAGGGGCAACA-3′), precursor of miR 302a (5′-GAAGCACTTACTTCTTTAGTTTC-3′) were provided from Exiqon (Vedbaek, Denmark). [score:1]
The most significant alignments with human miRNA were obtained with four pre-miRNA (pre-mir-302a, pre-let-7b, pre-mir-1267 and pre-mir-1296; E-value <0.1) and with the two miRNA (mir-365 and mir-31; E-value <0.1) Examples of alignment results show that for some candidates the seed region was perfectly aligned and some others had one or two nucleotide differences (Figure 1). [score:1]
Hoechst 33342 staining of nuclei (lane 1), specific signal of scramble miR (A; negative control), U6 small nuclear RNA (B; positive control), let-7b (C), mir-365 (D), pre-let-7b (E) and pre-mir-302a (F) provided by locked nucleic acid (LNA) probes (lane 2) and MitoTracker® Red CM-H [2]XRos staining of functioning mitochondria (lane 3) are represented in gray scale. [score:1]
Using locked nucleic acid (LNA) probes, we performed in situ hybridization to localized mir-365, mir-let-7b, pre-let-7b and pre-mir-302a within the cell. [score:1]
Among them, the mir-365, detected by in situ hybridization, was confirmed. [score:1]
We confirmed the intense co-localization of mir-365 in the mitochondria and some local areas in the nucleus (Figure 5 D). [score:1]
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11
[+] score: 20
The miRNAs expressed at the highest levels coincided with those reported by previous studies, and were similar to those expressed by NBC in our study, though several divergences emerged between CLL and NBC, such as the previously reported overexpression of miR-150-5p, miR-29a-3p, miR-155-5p, or miR-101-3p, underexpression of miR-181a-5p, or miR-181b-5p [14– 19], and others not firmly established yet, including the highly divergent miR-451a, miR-28-5p, miR-144-5p, miR-486-5p, or miR-486-3p, within the overexpressed, and miR-126-3p, miR-365a-3p, miR-199a-3p, or miR-582-5p, within the underexpressed. [score:13]
However, 41 miRNAs were differentially expressed between CLL and NBC according to the Student t test (cut-off 2-fold, p<0.05), being 29 overexpressed in CLL, including miR-150-5p, miR-29a-3p, miR-29b-3p, let-7a-5p, miR-26a-5p, miR-451a, miR-155-5p, miR-101-3p, miR-28-5p, miR-144-5p, miR-486-5p, or miR-486-3p, and 12 underexpressed, including miR-181a-5p, miR-222-3p, miR-126-3p, miR-365a-3p, miR-181b-5p, miR-199a-3p, or miR-582-5p (Table 1). [score:7]
[1 to 20 of 2 sentences]
12
[+] score: 19
Additionally, hsa-miR-365, hsa-miR-1238, hsa-miR-184 are all down-regulated in [ER−|PR−]HER2−, and up-regulated in [ER−|PR−]HER2+. [score:7]
Hsa-miR-365 is over-expressed in human breast cancer which down-regulates IL-6 in HeLa cells 27. [score:6]
Here we show that its expression could distinguish ER− tumors stratified by HER2 status, and have CXCL14 sharing the same expression pattern with hsa-miR-365, which together suggests the differential regulation of chemokines in breast cancer subtypes. [score:6]
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13
[+] score: 15
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-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Figure 8The Prdm1 targeting miRNAs miR-23b, miR-125a, miR-351, miR-30a/c/d, miR-182, miR-96, miR-98, miR-200b/c, and miR-365 are upregulated by HDI. [score:6]
In addition to miR-23b, miR-30a, and miR-125b, which, as we showed by qRT-PCR and miRNA-Seq, are upregulated by HDI, several other putative Prdm1 targeting miRNAs, including miR-125a, miR-96, miR-351, miR-30c, miR-182, miR-23a, miR-200b, miR-200c, miR-365, let-7, miR-98, and miR-133, were also significantly increased by HDI. [score:6]
org), we identified miR-125a, miR-125b, miR-96, miR-351, miR-30, miR-182, miR-23a, miR-23b, miR-200b, miR-200c, miR-33a, miR-365, let-7, miR-98, miR-24, miR-9, miR-223, and miR-133 as PRDM1/Prdm1 targeting miRNAs in both the human and the mouse. [score:3]
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14
[+] score: 13
For the first set of MSCs only 3 miRNAs (miR-324-3p, miR-494-3p, and miR-1260a) were observed to be statistically significant (p < 0.05) between passages 3 and 7. For the second set of MSCs, 7 miRNAs (let-7i, miR-25-3p, miR-106b-5p, miR-130b-3p, miR-199a-5p, miR-365a-5p, and miR-1260a) were statistically significant between passages 4 and 8. MiR-1260a was found to be significantly different between early and late passages for both MSC sets; however, it was upregulated at passage 7 for the first MSC set and downregulated at passage 8 for the second MSC set. [score:7]
Similar to the microarray results, 5 of the 10 miRNAs (miR-196b-5p, let-7i-5p, miR-22-3p, miR-193b-3p, and miR-365a-5p) were significantly downregulated in the cancer cell lines compared to early passage MSCs. [score:3]
Five of the miRNAs (miR-320c, miR-320d, miR-365a-3p, miR-494, and miR-1305) did not have detectable expression when using the platform. [score:3]
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15
[+] score: 13
The miRNAs hsa-miR-99a and hsa-miR-365 are downregulated in Lupus vulgaris [38], but were upregulated in blood of melanoma patients. [score:7]
Out of the 51 miRNAs that were deregulated in blood of melanoma patients four miRNAs, namely hsa-miR-99a, hsa-miR-365, hsa-miR-30a, and hsa-miR-146a, were deregulated in non-cancer skin diseases [37, 38]. [score:5]
The best classification accuracy has been obtained by using a subset that consists of 16 miRNAs including hsa-miR-186, hsa-let-7d*, hsa-miR-18a*, hsa-miR-145, hsa-miR-99a, hsa-miR-664, hsa-miR-501-5p, hsa-miR-378*, hsa-miR-29c*, hsa-miR-1280, hsa-miR-365, hsa-miR-1249, hsa-miR-328, hsa-miR-422a, hsa-miR-30 d, and hsa-miR-17*. [score:1]
[1 to 20 of 3 sentences]
16
[+] score: 11
In four FET placenta-specific miRNAs, there was no significant correlation between miRNA expression and maternal age, whereas there were weak correlations between expression levels of miR-125a-5p, miR-224-3p, miR-331-3p, miR-365a-3p, miR-518b, miR-518f-3p, and miR-543 and maternal age (Additional file 7: Table S5). [score:5]
The boxplots show the expression levels of miR-197-5p (a), miR-4697-5p (b), miR-4721 (c), miR-5006-5p (d), miR-575 (e), miR-6893-5p (f), miR-125a-5p (g), miR-1260b (h), miR-224-3p (i), miR-331-3p (j), miR-365a-3p (k), miR-495-3p (l), miR-518b (m), miR-518f-3p (n), miR-543 (o) and miR-7977 (p). [score:3]
Nine (miR-125a-5p, miR-224-3p, miR-331-3p, miR-365a-3p, miR-495-3p, miR-518b, miR-518f-3p, miR-543, and miR-7977) were significantly downregulated in FET placentae compared with SP, but not ET (Fig. 2 and Additional file 5: Figure S1). [score:3]
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17
[+] score: 10
Interestingly, in chicken all four miRNAs are predominantly expressed by red cells and gga-miR-365-3p is undetected in PBMCs (Figure S2). [score:3]
In mouse, the mature miRNAs encoded by mir-let-7f are predominantly expressed in hematopoietic cells, while the homolog of gga-miR-365-3p is ubiquitous and has been detected at low levels in most blood cells [45]. [score:3]
However, only the six miRNAs (miR-2954, gga-miR-2188-5p, gga-miR-365-3p, gga-miR-193b-3p, gga-miR-204 and mmu-miR-145a-5p) which compose Cluster 1 are found to be almost three-fold more abundant when concurrently considering R− and R+ animals (Table S2). [score:1]
These data are in agreement with the average number of sequence reads found in the plasma of R+ and R− animals for gga-miR-2188-5p (average 2.1 million reads), gga-let-7f-5p (average 143000 reads), gga-miR-365-3p (average 4600 reads) and gga-miR-2188-3p (average 1700 reads). [score:1]
As part of our validation of the procedure to obtain chicken plasma miRNAs (Figure 1), we profiled four miRNAs (gga-let-7f-5p, gga-miR-365-3p, gga-miR-2188-5p and gga-miR-2188-3p) by RT-qPCR from whole chicken blood, PBMCs, plasma and red cells. [score:1]
The miRNAs were selected among those found differentially abundant in the Condition comparison (gga-miR-204, gga-miR-2188-5p and gga-miR-365-3p), in the Line comparison (gga-miR-2188-3p, and gga-miR-122-5p) or in both (gga-let-7f-5p). [score:1]
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[+] score: 10
Upregulated miRNA-365 has shown inhibitory effect against IL-6 signaling by binding at its 3′UTR in tuberculosis infection (Song et al., 2015). [score:6]
Altered expression of miRNA-365, miRNA-483-5p, miRNA-22, miRNA-29c, miRNA-101, and miRNA-320 are reported in tuberculosis and affect the mitogen-activated protein kinases (MAPK) and transforming growth factor beta (TGF-β) signaling to develop tuberculosis infection (Zhang et al., 2013). [score:3]
MicroRNA-365 in macrophages regulates Mycobacterium tuberculosis -induced active pulmonary tuberculosis via interleukin-6. Int. [score:1]
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[+] score: 10
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
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20
[+] score: 9
Both oncogenic miRNAs and tumor suppressive miRNAs have been demonstrated and described in colon carcinogenesis and progression, such as upregulated miR-135, miR-21, miR-17-92, and miR-196a, and downregulated miR-34, miR-195, and miR-365 [9]– [13]. [score:9]
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[+] score: 9
42) 13 hsa-mir-199b dbDEMC, HMDD, miR2Disease 38 hsa-mir-206 dbDEMC 14 hsa-mir-181a dbDEMC, miR2Disease 39 hsa-mir-192 dbDEMC 15 hsa-mir-29a dbDEMC, HMDD, miR2Disease 40 hsa-mir-335 literature 16 hsa-let-7e dbDEMC 41 hsa-mir-365 literature 17 hsa-mir-107 HMDD 42 hsa-mir-30a miR2Disease 18 hsa-mir-18a higher RWRMDA (No. [score:9]
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[+] score: 9
First, the expression patterns of several miRNAs (miRNA-221, miRNA-222, and miRNA-365) display mechanoresponsiveness [71, 72], while a mechanoregulatory protein, integrin alpha-5, the levels of which are correlated with BMI, was identified as a target of miRNA-25 that is down-regulated in OA specimens [70]. [score:9]
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23
[+] score: 9
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-15a, hsa-mir-16-1, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
Similarly, 52 miRNAs, such as hsa-miR-202, hsa-miR-365, and hsa-miR-412 have active splice sites within a pri-miRNA, which can be a regulatory factor for their expression in tissue- and development-specific manner (Melamed et al. 2013). [score:5]
For instance, human miR-365 has two copies, one with an active splice site, whereas the other one is intronic; this suggests regulator modulation of the expression of paralogous miRNAs (Melamed et al. 2013). [score:4]
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24
[+] score: 9
It has been reported that miR-365 decreases IL-6 expression by repressing mRNA translation, without affecting IL-6 mRNA levels[43]. [score:5]
The expression of miR-365, however, was not changed by EDC4 or Dcp1a knockdown (Fig 7A). [score:4]
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25
[+] score: 9
To validate the accuracy of our heatmap results, we performed qPCR to confirm the expression levels of the top up-regulated miRNAs (such as miR365a-3p, miR-2277-3p, and miR-184-3p) and down-regulated miRNAs (such as miR-21-5p, miR-136-3p, and miR-127-3p) (Fig.   1g). [score:9]
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26
[+] score: 7
As expected, most majority of the miRNAs, either upregulated in the cancer tissues, such as miR-223-3p [61], miR-421 [62], miR-424-5p [63], miR-1260b [64] etc, or downregulated in the penile cancer, such as miR-205-5p [65], miR-211-5p [65– 66], miR-365-3p [67] and miR-1247 [68] etc, were entitled the similar roles in carcinogenesis of bladder cancer, retinoblastoma, breast cancer, nasopharyngeal cancer, pancreatic cancer and several other cancer types [61– 68]. [score:7]
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[+] score: 7
As shown in the heat map, compared with sample on PID 0, most miRNAs were down-regulated in sample on PID 4, whereas only few miRNAs were differentially expressed in sample on PID 7. Compared with sample on PID 4, a majority of miRNAs were up-regulated in sample on PID 7. To validate the Solexa sequencing results, qRT-PCR was performed separately to investigate the relative expression levels of 5 randomly selected DE miRNAs (ssc-miR-424-3p, ssc-miR-542-5p, ssc-miR-365-5p, ssc-miR-450b-5p, ssc-miR-450a). [score:7]
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[+] score: 7
In cSCC most of the altered miRNAs are downregulated (miR-125b, miR-34a, miR-214, miR-124, miR-361, miR-193b, miR-365a, miR-20a, miR-199a) [19– 25] whereas only a small number of miRNAs have been found to be upregulated and act as onco-miRNAs, being involved in angiogenesis, colony formation, migration and invasion, and metastatic spread (miR-365, miR-9, miR-184, miR-21, miR-31, miR-135b, miR-205, let-7a) [25– 34]. [score:7]
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29
[+] score: 6
Luciferase reporter analysis revealed that the activity of reporter containing wild type 3’UTR of KLF4 was significantly suppressed (about 40% reduction) by miR-29, but not by miR-365 (Fig 7C). [score:3]
miR-365a was selected as negative control, since there is no binding site of miR-365a in the cloned DNA fragment. [score:1]
Luciferase reporters were co -transfected with miR-29 mimic or miR-365 mimic, an unrelated miRNA as negative control. [score:1]
#:C300650-07) or hsa-miR-365a-3p mimic (Dharmacon, Cat. [score:1]
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[+] score: 6
Qin B. Xiao B. Liang D. Xia J. Li Y. Yang H. MicroRNAs expression in ox-LDL treated HUVECs: MiR-365 modulates apoptosis and Bcl-2 expression Biochem. [score:4]
Furthermore, several other microRNAs are also shown to be important in regulating endothelial cell apoptosis, including miR-19a, miR-26a, miR-495, miR-US25-1, miR-223, let-7, miR-126, miR-21, miR-590-5p, miR-513a-5p, miR-23a, miR-365, etc. [score:2]
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[+] score: 6
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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-204, hsa-mir-205, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-149, hsa-mir-150, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-365b, hsa-mir-370, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-335, hsa-mir-133b, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-574, hsa-mir-605, hsa-mir-33b, hsa-mir-378d-2, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-378j
Further, miR-193b and miR-365, also present in milk, were shown to control lipid synthesis, upregulating brown fat differentiation via enhancing expression of Runt-related transcription factor 1 translocated to 1 (Runx1t1) [166]. [score:6]
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[+] score: 6
The lacking of HNF4 α expression in the liver of young adult mice (Hnf4α-Liv KO) determined the downregulation of some miRs, including miR-193a that is in cluster with miR-365 on the chromosome 11 of Mus musculus [5]. [score:6]
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[+] score: 6
For example, miR-365 is up-regulated by ox-LDL-C, leading to reduced expression of BCL2, an antiapoptotic gene, in arterial endothelial cells [22]. [score:6]
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34
[+] score: 6
Both miR-193b and miR-365a could acted as a tumor suppressor in the epidermis by directly targeting KRAS oncogene [79]. [score:6]
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35
[+] score: 6
Overexpression of miR-365a-3p had a similar effect, as did miR-34a-5p, -148a-3p, and -183-5p, on the suppression of endogenous FOXP1 in SKW6.4 cells (Fig. 5E). [score:5]
Likewise, disruption of the miR-183-5p, miR-34a-5p, or miR-148a-3p site, but not the miR-365a-3p site, attenuated the repression of FOXP1 3′UTR–mediated luciferase activity (Fig. 5C). [score:1]
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36
[+] score: 5
Inhibition of miR-193a/b and/or miR-365 in mouse primary brown pre-adipocytes impairs brown adipogenesis in vitro [14]. [score:3]
However, miR-193b null mice, that are also deficient in miR-365, have normal BAT development, differentiation and function [24]. [score:2]
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37
[+] score: 5
The target gene of miR-365 was predicted by TargetScan, using the context++ score system, as has been instructed before [21]. [score:5]
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38
[+] score: 5
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-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Of the 10 miRNAs examined, all except miR-365 and miR-151 were differentially expressed between naïve and infected mice by 6–8 weeks post infection (Fig. 1, Table S2). [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
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39
[+] score: 5
BLC2 has been examined with several targeted miRNAs, including miR-491, miR-143, miR-148a, miR-365, miR-1915, miR-204, and miR-125b [4– 6, 8, 29– 31]. [score:3]
Several miRNAs, including miR-124 [2], miR-195 [3], miR-148a [4], miR-365 [5], miR-125b [6], miR-129 [7], miR-143 [8], and miR-203 [9], have been linked to apoptosis through regulation of genes such as BCL2 and PUMA, a member of the Bcl-2 family, involved in pro-apoptosis [1, 4, 6, 8, 9]. [score:2]
[1 to 20 of 2 sentences]
40
[+] score: 4
miR-365 is clustered with miR-193b which shows similar expression patterns to miR-365 in our system (Tables 2 and 3 ), thus suggesting that these miRNAs may be co-regulated. [score:4]
[1 to 20 of 1 sentences]
41
[+] 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-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, 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-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, 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-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-145 and miR-365 were specifically expressed in DRG (Fig. 3a). [score:3]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
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42
[+] 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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-204, hsa-mir-210, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-365b, hsa-mir-369, hsa-mir-370, hsa-mir-371a, hsa-mir-375, hsa-mir-378a, hsa-mir-133b, hsa-mir-423, hsa-mir-448, hsa-mir-429, hsa-mir-486-1, hsa-mir-146b, hsa-mir-181d, hsa-mir-520c, hsa-mir-499a, hsa-mir-509-1, hsa-mir-532, hsa-mir-33b, hsa-mir-637, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-509-2, hsa-mir-208b, hsa-mir-509-3, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-371b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
Downregulates C/EBPα and PPARγ[73] miR-365 Brown fat differentiation[202] miR-369 FABP4. [score:4]
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43
[+] score: 3
Expression of several miRNAs related to BAT metabolism such as miR-26a, miR-27a, miR-93, miR-193b, miR-365a, and miR-445 were altered in response to the diet in both genotypes while no effect of genotype was observed (Figure S1). [score:3]
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44
[+] score: 3
Recent studies have demonstrated that the abnormal expression of certain miRNAs, including miR-145 (8), miR-203 (9) and miR-365 (10), is involved in colon cancer. [score:3]
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45
[+] score: 3
The expression profile of mature miRNAs for let-7a, let-7b, let-7c, let-7e, let-7f, let-7g and let-7i, miR-211, miR-27b, miR-26b, miR-126, miR-30d, miR-365, miR-150, miR451a and miR451a. [score:3]
[1 to 20 of 1 sentences]
46
[+] score: 3
Of these, nine miRNAs (hsa-miR-326 [21], hsa-miR-211 [22], [23], hsa-miR-10b [32], hsa-miR-365 [32], hsa-miR-10a [32], hsa-miR-503 [32], hsa-miR-335* [30], hsa-miR-331-3p [30] and has-miR-199a-5p [30]) were expressed at higher levels in abdominal, rather than gluteal, adipose tissue (Table S1). [score:3]
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47
[+] score: 3
Yang et al. [81] used immunohistochemical methods to study breast tumor subtypes and found that there is expression differences on hsa-miR-365, hsa-miR-1238 and hsa-miR-184. [score:3]
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48
[+] score: 3
We found two miRNA—target interactions (UBAC2—miR-365a-3p and SNAPC4—miR-3661) which were experimentally validated by the CLIP-seq method (Supplementary Table 3). [score:3]
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49
[+] score: 2
Importantly, only one of these miRNAs slightly increased Salmonella infection (miR-365, 1.8-fold increase; S1 Table). [score:1]
Of note, the mature miR-365a-3p and miR-365b-3p have the same sequence; in miRBase 13, this miRNA was named miR-365 (result is shown in italic). [score:1]
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50
[+] score: 2
We identified that miR-148a, miR-26b, miR-132, miR-365 and miR-1908 were highly expressed in mature adipocytes with over 5-fold compared to SVCs/hMSCs-Ad. [score:2]
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51
[+] score: 2
Some microRNAs have the ability to negatively regulate the activity of PR domain containing 16 (PRDM16), including miR-133, miR-193b, and miR-365 [74– 76]. [score:2]
[1 to 20 of 1 sentences]
52
[+] score: 2
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
[1 to 20 of 1 sentences]
53
[+] score: 2
Bcl-2 was also regulated by other miRNAs, such as miR-204, [87] miR-148a [88] and miR-365. [score:2]
[1 to 20 of 1 sentences]
54
[+] score: 1
0013219hsa-miR-301a-3p0.2070.0048517hsa-miR-45000.4130.0096213hsa-miR-451b0.2100.0055917hsa-miR-36540.4150.004007hsa-miR-1070.2160.0001010hsa-miR-223-3p0.4160.00199Xhsa-miR-196b-3p0.2260.000837hsa-miR-3607-5p0.4210.004125hsa-miR-5581-3p0.2299.8E-051hsa-miR-93-3p0.4220.001297hsa-miR-44170.2300.001241hsa-miR-24-3p0.4270.037889hsa-miR-185-5p0.2390.0136722hsa-miR-365a-3p0.4330.0003016hsa-miR-12750.2400.013796hsa-miR-1260b0.4340. [score:1]
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55
[+] score: 1
LPS treatment caused significant increase in abundance of miR-146a-5p, miR-574-5p and decreased abundance of miR-1-3p, miR-133a-3p, miR-206, and miR-365a-3p/365b-3p. [score:1]
[1 to 20 of 1 sentences]
56
[+] score: 1
Severe miRNAs have been identified to be responsive for hypoxia, such as miR-210, miR-517a/b, miR-424, miR-365, etc. [score:1]
[1 to 20 of 1 sentences]
57
[+] score: 1
An increasing number of studies have indicated that miRNAs participate in the pathogenesis of osteoarthritis, with confirmation for miR-139, miR-140, miR-23a-3p and miR-365 [6– 9]. [score:1]
[1 to 20 of 1 sentences]
58
[+] score: 1
The miRNAs that have been identified as associated with lung cancer include miR-210 (26), miR-365 (27) and miR-449 (28), indicating an association between miRNA and NSCLC. [score:1]
[1 to 20 of 1 sentences]
59
[+] score: 1
Of these, while 24 miRNAs including miR150, miR199a-5p, miR-223, miR-28-5p, miR-451, were significantly depleted, 10 miRNAs including miR-34a, miR-155, miR-193b, miR-365, miR-551b, displayed induction. [score:1]
[1 to 20 of 1 sentences]
60
[+] score: 1
Six modulated microRNAs were then selected for real-time PCR validation, which confirmed significant induction of miR-30a-3p and-5p, miR-30c-5p and miR-30c2-3p and miR-365a-5p in keratinocytes from aged skin, whereas miR-4443 was significantly reduced in the aged sample (Figure 1B). [score:1]
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61
[+] score: 1
Scare bar = 50 μm To explore whether circHIPK3 can function as “miRNA sponge” in CRC cells, we selected the top ten (miR-599, miR-93-3p, miR-365a-5p, miR-365b-5p, miR-421, miR-570-3p, miR-597-5p, miR-7, miR-1207-3p, miR-124-5p) candidate miRNAs through CircNet database [21]. [score:1]
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62
[+] score: 1
90 Down 3.84E-18 hsa-miR-4448 2.45 Up 1.66E-04 hsa-miR-1250 −5.71 Down 2.05E-169 hsa-miR-4426 2.23 Up 3.53E-05 hsa-miR-139-5p −5.46 Down 3.71E-25 hsa-miR-720 2.08 Up 1.21E-05 hsa-miR-335-5p −5.26 Down 2.00E-41 hsa-miR-4485 1.71 Up 6.14E-08 hsa-miR-362-3p −5.01 Down 3.36E-10 hsa-miR-877-5p 1.68 Up 1.92E-82 hsa-miR-1255a −4.92 Down 1.25E-62 hsa-miR-3679-5p 1.45 Up 5.53E-04 hsa-miR-3622a-5p −4.83 Down 4.30E-09 hsa-miR-21-3p 1.40 Up 7.87E-13 hsa-miR-1293 −4.67 Down 2.87E-08 hsa-miR-2116-3p −4.64 Down 3.67E-14 hsa-miR-365a-3p −4. [score:1]
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63
[+] score: 1
As some miRs have been identified as being responsive to one or either of these factors, such as miR-222 or miR-365 for biomechanics [22, 23] and miR-103 or miR-143 for obesity [24], it is not surprising that miRs profiles may vary between OA patients depending on their OA phenotypes [25]. [score:1]
[1 to 20 of 1 sentences]
64
[+] score: 1
Studies of exosomes from MLC supernatants revealed the presence of inflammatory microRNA, including miR-146a, miR-155, miR-21, miR-30b, miR-365, and Let-7a. [score:1]
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65
[+] score: 1
miR-22, miR-25, miR-197, miR-365, miR-483-5p, miR-590-5p, and miR-885-5p are yet the most promising candidates since these miRNAs were validated for discrimination of TB and healthy controls in two studies (see Table  2). [score:1]
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66
[+] score: 1
Other miRNAs from this paper: hsa-mir-365b
Guo S. L. Ye H. Teng Y. Wang Y. L. Yang G. Li X. B. Zhang C. Yang X. Yang Z. Z. Yang X. Akt-p53-miR-365-cyclin D1/cdc25A axis contributes to gastric tumorigenesis induced by PTEN deficiecy Nat. [score:1]
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67
[+] score: 1
21 hsa-miR-140-3p −1.22 hsa-miR-450a −1.23 hsa-miR-210 †† −1.24 1.48 hsa-miR-26b −1.25 hsa-miR-10b −1.25 −1.25 hsa-miR-101 −1.26 −1.28 hsa-let-7c −1.28 hsa-miR-98 −1.29 −1.21 hsa-miR-23a −1.30 hsa-miR-22* −1.34 −1.42 hsa-miR-337-3p −1.38 −1.23 hsa-miR-31 −1.39 −1.34 hsa-miR-365 −1.43 −1.38 hsa-miR-137 −1.46 −1.45 hsa-miR-494 −1.55 hsa-miR-29b −1.82 −1.93 hsa-miR-221 † −1.88 −1.84 hsa-miR-29c −2.33 hsa-let-7i 1.21 hsa-miR-125b † −1.24 hsa-miR-195 −1. [score:1]
[1 to 20 of 1 sentences]
68
[+] score: 1
Several microRNAs including miR-29, miR-365, and miR-17-92 [14, 19] control tumor cell proliferation, invasion and survival. [score:1]
[1 to 20 of 1 sentences]
69
[+] score: 1
These include miR-145-5p [20, 21], miR-141-3p [21, 22], miR-27b-3p [21, 81], miR-106b-5p, miR-93-5p [21] miR-148a-3p, miR-193a-3p [22, 81], miR-135a-5p, miR-374b-5p, miR-29c-3p, miR-365a-3p [22], let-7a-5p, miR-515-3p [24], and miR-34c-3p [81]. [score:1]
[1 to 20 of 1 sentences]
70
[+] score: 1
Identified lung cancer related microRNAs include mir-210 [42], mir-365 [43], mir-449c [44], etc. [score:1]
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