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11 publications mentioning rno-mir-224

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-224. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 142
Other miRNAs from this paper: rno-mir-221, rno-mir-222
We also found significantly lower miR-224 expression levels during the study period in patients with persistent disease, progressive disease, and fatal disease progression (p = 0.001, p = 0.002, and p = 0.0001, resp. [score:9]
After logarithmic transformation, the t-test and ANOVA were used to measure differences in miR-224 expression levels in different subgroups based on clinical/pathological variables (female versus male, different stages at diagnosis, lower versus higher Ct levels at diagnosis, biochemically cured status versus persistent disease, disease progression versus a stable disease, and death versus alive) and molecular features (RET/ RAS status). [score:7]
Our Kaplan-Meier analysis showed that patients with tumors showing a low miR-224 expression levels were likely to have a significantly shorter overall survival than those with a high miR-224 expression levels, strongly suggesting that low miR-224 expression levels is a marker of a poor prognosis in patients with MTC. [score:7]
Our present findings confirmed as much, since miR-224 expression levels were significantly lower in patients with distant metastases, persistent disease, and disease progression during their follow-up. [score:7]
Judging from our data, miR-224 acts as an oncosuppressor-miR in MTC and lower miR-224 expression levels serves as an independent prognostic molecular marker of a more aggressive disease that can identify patients at risk of progression and MTC-related death. [score:7]
It may depend on the expression of miR-224 target genes in various cell types, since it can promote or inhibit cancer cell growth, depending on the histotype of the malignancy concerned. [score:7]
In the light of the above findings, and as demonstrated for other miRNAs, such as miR-221 and miR-222 [35- 37], miR-224 seems to have a dual mode of action that depends on the type of cancer involved: it acts as an onco-miR in some cancers and as an oncosuppressor-miR in others, suggesting that different molecular targets and networks are regulated by miR-224 in different neoplastic scenarios. [score:6]
It is also worth mentioning the recent finding that, although miR-224 upregulation is a known negative prognostic factor in HCC, the high miR-224 phenotype in this cancer has been found associated with a better response to sorafenib, an inhibitor of several tyrosine kinase receptors, such as RET, RAF kinase, and vascular endothelial growth factor (VEGF) receptor, that is also used in MTC [34]. [score:6]
The expression levels of miR-224 were significantly associated with patients' main clinical and pathological findings and with their outcome: there was a statistically significant negative association between miR-224 expression level and serum Ct level at diagnosis: the higher the former, the lower the latter (p = 0.03, r = −0.3; rank correlation). [score:5]
As expected from the Kaplan-Meier analysis and log-rank test, patients with a low miR-224 expression tended to have a shorter overall survival than those with a high miR-224 expression levels (p = 0.005; log-rank test) (Figure 2). [score:5]
In glioblastoma, miR-224 overexpression increases radiation sensitivity, thus improving outcomes, and patients with high miR-224 expression levels reportedly have a better overall survival [20]. [score:5]
Stage at diagnosis and miR-224 expression levels correlated independently with disease progression (OR 29.8, 95%CI 3.7–243.3 and OR 0.7, 95%CI 0.5–0.9, resp. [score:5]
We also found a significant positive association between RAS-mutated status and miR-224 expression levels: the presence of RAS mutations was associated with higher miR-224 levels (p = 0.007; t-test), and the association was confirmed after the exclusion of RET -positive patients, too (p = 0.03; t-test), confirming that sporadic RAS+/RET−MTC is a less aggressive phenotype (Figure 3). [score:4]
We found no significant association between the presence of RET mutations and miR-224 expression levels. [score:4]
Our findings also support the positive prognostic role of RAS mutation found in a previous multicenter study [8]: all of our RAS-mutated patients were alive, and they had a less aggressive MTC phenotype and higher levels of miR-224 expression (although, based on our data, we cannot rule out the possibility of such associations being accidental). [score:4]
Yu et al. found miR-224 upregulation and AKT activation synergistically associated with tumor progression in hepatocellular carcinoma (HCC) [25]. [score:4]
The present study showed that, together with the presence of RAS mutations, higher miR-224 expression levels are also molecular markers of a favorable prognosis in sporadic MTC. [score:4]
Finally, our multivariate logistic regression analysis demonstrated that lower serum Ct levels at diagnosis and higher levels of miR-224 expression correlated independently with biochemical cure (OR 0.999, 95%CI 0.9987–0.999 and OR 1.4, 95%CI 1.06–1.8, resp. [score:3]
More importantly, as already shown in glioblastoma tissues, we ascertained that miR-224 expression levels was significantly associated with patient survival. [score:3]
In association with serum Ct levels at diagnosis and stage of disease, miR-224 emerged from our multivariate analysis as an independent prognostic marker. [score:3]
On the other hand, Mencia et al. demonstrated that miR-224 underexpression leads to insensitivity towards methotrexate, favoring a resistant phenotype [18]. [score:3]
), but only miR-224 levels correlated independently with disease-related death (OR 0.3, 95%CI 0.1–0.6). [score:3]
The aims of the present study on a large series of familial and sporadic cases of MTC were as follows: (a) to confirm our previous findings concerning miR-224 expression and its relationship with patient outcome; (b) to elucidate its relationship with the main molecular events responsible for MTC. [score:3]
We initially examined the clinical/pathological differences in relation to serum Ct levels at diagnosis, then we considered the differences in miR-224 expression level in relation to the following: (a) clinical/pathological findings (CT level at diagnosis, nodal and distant involvement, and TNM stage); (b) patient's outcome; and (c) somatic RET and RAS mutations in sporadic MTCs. [score:3]
To our knowledge, this is the first study to explore the expression profile of miR-224 in a large cohort of MTC patients, assessing its relationship with clinical, pathological, and molecular features. [score:3]
The literature currently provides little or no information on miR-224 expression levels in neuroendocrine tumors. [score:3]
We found lower miR-224 values in patients with advanced stage disease at diagnosis (p = 0.001; ANOVA): patients with nodal and distant metastases at diagnosis had significantly lower miR-224 levels (p = 0.005 and p = 0.0001, resp. [score:3]
Lan et al. found that HCV -induced low autophagy could lead to a high miR-224 expression with a tumorigenic effect [16]. [score:3]
Some surveys recently suggested that miR-224 overexpression could play a significant part in promoting tumor cell proliferation and migration, with an oncogenic role. [score:3]
miR-224 is a microRNA commonly dysregulated in most human cancers that affects crucial cellular processes and resides in chromosome Xq28 [22]. [score:2]
These findings indicate that miR-224 has an indispensable role in cell proliferation, but also in the apoptosis of cancer cells, and the crucial balance between these two processes decides the miR-224 phenotype identifiable in tumor cells [22]. [score:1]
A previous study of ours on a small series of 34 MTC patients found that miR-224 could represent a prognostic biomarker associated with a better outcome [11]. [score:1]
The Kaplan-Meier method was used to estimate the survival rates, and the log-rank test was used to assess the survival differences between the groups (the miR-224 levels were dichotomized as “high” or “low” based on the mean value of the variable). [score:1]
miR-224 is an independent prognostic marker in cervical cancer and lung cancer too [17, 19, 32]. [score:1]
Huang et al. suggested that miR-224 might have an important role in promoting the onset and progression of bone metastases from breast cancer [31]. [score:1]
A rank correlation analysis was used to study the influence of miR-224 on CT levels at diagnosis. [score:1]
2.3. miR-224 Quantitative Real-Time Polymerase Chain Reaction. [score:1]
The intriguing role of miR-224 has yet to be fully elucidated. [score:1]
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2
[+] score: 47
Schematic representation of our hypothesis (C) and results (D) which suggest a siAQP4 -induced up-regulation of miR224 which mediates the down-regulation of his target Cx43. [score:9]
siAQP4 -induced down-regulation of Cx43 could be in part due to miR224 increased expression. [score:6]
Interestingly, siCx43 treatment induced a down-regulation of miR19a and miR224, which in turn, were not able to decrease AQP4 expression; *p < 0.05; values are represented as mean ± SEM. [score:6]
The reduction of Cx43 expression in siAQP4 treated animals relative to control animals was associated with up-regulation of miR224. [score:6]
In summary, we demonstrate for the first time that AQP4 decrease after siAQP4 induces an increase of miR224 and miR19a expression with decreases in Cx43 levels and astrocyte connectivity. [score:3]
Therefore, the level of expression of AQP4 and Cx43 possibly affects the miR224 and miR19a with an opposite effect: a decrease of AQP4 is associated with an increase of both miRNAs and decrease of Cx43 is linked with a decrease of these miRNAs (Fig. 8). [score:3]
Figure 8Modulation of miR19a, miR23a, miR130a, miR224, miR381 and miR384-5p expression after siAQP4 and siCx43 treatment. [score:3]
However, we observed a significant 36% increase in the expression of miR224 in the ipsilateral cortex of siAQP4 -treated animals relative to siGLO controls (Fig. 8A). [score:3]
We found significant decreased expression of miR19a (44%) and miR224 (61%) in the ipsilateral cortex of siCx43 animals compared to siGLO control animals (Fig. 8B). [score:2]
However, siAQP4 and siCx43 injections appear to affect levels of miR224 and miR19a in opposite directions with an increase in the siAQP4 -treated cortex versus a decrease in the siCx43 brain. [score:2]
We chose to study 6 miRNAs, among those most conserved between species: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p. [score:1]
Therefore, interventions such as siAQP4 or miR224 and miR19a could be used as potential treatments to decrease levels of Cx43 in ALS and epilepsy. [score:1]
We chose the most conserved miRNAs between species and selected 6 miRNAs: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p (see Table 1). [score:1]
AQP4 Cx43 Homo sapiens Mus musculus Rattus norvegicus Homo sapiens Mus musculus Rattus norvegicus miR19a ● ● ● ● ○ ○ ○ miR23a ● ● ● ● ○ ○ ○ miR130a shown to repress transcriptional activity of AQP4 M1 promoter* ● ● ● miR224 ● ● ● ● miR381 ● ● ● ● miR384-5p ● ● ● ● ○ ○ ○● based on microrna. [score:1]
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3
[+] score: 36
As shown in Figure 3C, miR-224 was strongly up-regulated in KRT-19 positive lesions (150-fold) compared to normal liver, supporting the notion that the increased miR-224 expression found in experimental and human HCC is most likely the consequence of its accumulation when autophagic machinery is deregulated. [score:6]
Recently, it was reported that inhibition of autophagy in hepatitis B -associated human HCCs is responsible for the strong accumulation of miR-224 - one of the most up-regulated miRs in human cancer [23, 24] - in these tumors [25]. [score:6]
Indeed, our data show a drastic upregulation of miRNA-224 in those subset of nodules which are more aggressive and develop HCC. [score:4]
Importantly, miRNA-224, involved in cell proliferation, migration and invasion [32], is one of the most up-regulated miRs in rodent and human HCC [21- 23, 24]. [score:4]
A recent study demonstrated that inhibition of autophagy in HBV -associated human HCCs is the mechanism responsible for the strong accumulation of the mature form miR-224 in these tumors [25]. [score:3]
Another relevant finding of the present work is the association between high miR-224 expression and autophagy impairment. [score:3]
miR-224 expression is reported as fold-change relative to age-matched controls; ***P<0.0001. [score:3]
C. qRT-PCR analysis of miR-224 expression in KRT-19 [+] nodules. [score:3]
MiR-224 is highly expressed in KRT-19 positive nodules. [score:2]
Therefore, we investigated the expression of miR-224 in KRT-19 [+] preneoplastic lesions. [score:1]
Analysis of mRNA levels of autophagy -associated genes and miRNA-224. [score:1]
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4
[+] score: 25
Upregulation of miR-224-5p has been found to occur as part of the protective adaptive response of hepatocytes during acetaminophen -induced toxicity, and this upregulation of miR-224-5p was associated with suppression of drug metabolizing enzyme levels [47]. [score:9]
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p demonstrated more abundant expression and a two-fold or greater significant increase in expression with Cd treatment. [score:5]
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p were more abundantly expressed and demonstrated a two-fold or greater increased expression in the Cd-treatment group. [score:5]
We used real-time PCR to confirm the increased expression of miR-21-5p, miR-34a-5p, mir-146b-5p, miR-224-5p, miR-3084a-3p, and miR-3084c-3p in the renal cortices from Cd -treated animals versus the saline controls. [score:3]
Selected miRNAs that demonstrated a statistically significant (p ≤ 0.05) altered expression using µParaflo™ microRNA microarray were validated using the following TaqMan [®] Advanced miRNA assays: miR-21-5p (rno481342_mir), miR-34a-5p (rno481304_mir), miR-146b-5p (rno480941_mir), miR-224-5p (rno481010_mir), miR-3084a-3p (rno481040_mir), miR-3084c-3p (rno481313_mir), and miR-455-3p (rno481396_mir). [score:2]
As shown in Figure 3, real-time PCR demonstrated a significant increase in the Cd -treated group for the following miRNAs: a 2.7-fold increase in miR-21-5p (Figure 3A), a 10.8-fold increase in miR-34a-5p (Figure 3B), a 2-fold increase in miR-146b-5p (Figure 3C), a 10.2-fold increase in miR-224-5p (Figure 3D), a 2.4-fold increase in miR-3084a-3p (Figure 3E), and a 3.3-fold increase in miR-3084c-3p (Figure 3F). [score:1]
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5
[+] score: 18
Finally, we find miR-224, associated with a human chromosome fragile site on Chr-Xq28 [18], is up-regulated in ccRCC and predicted to target ERBB4, a member of the EGFR family, a potential tumor suppressor known to be strongly down-regulated in ccRCC [78]. [score:11]
For instance, loss of miR-149, miR-200c and mir-141 causes gain of function of oncogenes (KCNMA1, LOX), VEGFA and SEMA6A respectively and increased levels of miR-142-3p, miR-185, mir-34a, miR-224, miR-21 cause loss of function of tumor suppressors LRRC2, PTPN13, SFRP1, ERBB4, and (SLC12A1, TCF21) respectively. [score:3]
As the p-values in Figure 4 indicate, we validate a strong anti-correlation signature between mRNA levels of (KCNMA1, LOX), VEGF, SEMA6A, (LRRC2, PTPN13), SFRP1, ERBB4, SLC12A1 and TCF21, and their identified regulators: miR-149, miR-200c, mir-141, miR-142-3p, miR-185, mir-34a, miR-224 and miR-21 respectively. [score:2]
In Figure 3B-E, we plot the qRT-PCR expression levels of ERBB4, SFRP1, SLC12A1 and VEGFA versus Agilent chip measured levels of their regulatory microRNA (miR-224, miR-34a, miR-21 and miR-200c) for the twelve samples of Figure 3A. [score:2]
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6
[+] score: 11
miR-224, let-7a, and let-7d were downregulated in colon cancer tissues, and upregulation of miR-224 or let-7a attenuated colon cancer growth [52– 55]. [score:7]
The upregulated miRNAs in the colon tissues of UC rats changed by HM were miR-149-5p, miR-351-5p, let-7d-5p, miR-98-5p, let-7a-5p, miR-3559-5p, let-7f-1-3p, miR-3596b, miR-224-5p, miR-411-3p, miR-184, miR-26b-3p, and miR-92b-3p. [score:4]
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7
[+] score: 9
Among them, 12 miRNAs (rno-miR-10b-5p, rno-miR-122-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-199a-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-208b-5p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p) were significantly upregulated(p<0.01, fold-change >1) compared to the control group and only rno-miR-208a-3p were significantly downregulated (p<0.01, fold-change <-1) (Fig 3). [score:6]
Meanwhile, rno-miR-10b-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p were reported for the first time to be differentially expressed in HF tissue. [score:3]
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8
[+] score: 8
The expression levels of 12 miRNAs, including miR-139-3p, miR-204, miR-760, miR-432, miR-524-5p, miR-136, miR-548d-3p, miR-206, miR-214, miR-383, miR-224, and miR-887 were significantly lower, whereas the expression level of miR-146a was significantly higher, in Jurkat cells after being cultured with TNF-α for 7 days (fold change > 4, p < 0.05, Fig.   1b). [score:5]
Lu MC Lai NS Chen HC Yu HC Huang KY Tung CH Decreased microRNA(miR)-145 and increased miR-224 expression in T cells from patients with systemic lupus erythematosus involved in lupus immunopathogenesisClin Exp Immunol. [score:3]
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9
[+] score: 5
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
For example, miRNA-503, miRNA-224 and miRNA-383 are expressed almost exclusively in mouse granulosa cells and oocytes [68], [72], whereas a large number of miRNAs are differentially expressed in bovine ovarian cortex, cumulus cells and corpus luteum [60]. [score:5]
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10
[+] score: 5
Over-expressed miR-224 promotes the progression of cervical cancer via targeting RASSF8. [score:5]
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11
[+] score: 1
It has been reported by other investigators that SMAD4 has been targeted by many microRNAs, e. g. miR-224 for cell proliferation and function through TGF-β pathway. [score:1]
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