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5 publications mentioning hsa-mir-1226

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1226. 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: 93
*Statistically significant results, p < 0.05 Table 4 Change of mirtronic miRNA expression levels in response to the overexpression of splicing factors Overexpressed splicing factorChange of mirtronic miRNA expression levels, folds (p value) miR-1226 miR-1227 miR-1229 SRSF1 (3.2 ± 0.6-fold)1.5 ± 0.6 (p = 0.23)−1.1 ± 0.4 (p = 0.47)1.7 ± 0.4 [a] (p = 0.05) SRSF2 (1.6 ± 0.5-fold)1.5 ± 0.8 (p = 0.15)1.9 ± 0.7 [a] (p = 0.008)1.4 ± 0.3 [a] (p = 0.008) A significance level of 0.05 was applied as a cutoff value [a]Statistically significant results Overall, our results lead to a conclusion that altered expression of a particular SF may affect the levels of mirtronic miRNAs in the cell. [score:11]
*Statistically significant results, p < 0.05 Table 4 Change of mirtronic miRNA expression levels in response to the overexpression of splicing factors Overexpressed splicing factorChange of mirtronic miRNA expression levels, folds (p value) miR-1226 miR-1227 miR-1229 SRSF1 (3.2 ± 0.6-fold)1.5 ± 0.6 (p = 0.23)−1.1 ± 0.4 (p = 0.47)1.7 ± 0.4 [a] (p = 0.05) SRSF2 (1.6 ± 0.5-fold)1.5 ± 0.8 (p = 0.15)1.9 ± 0.7 [a] (p = 0.008)1.4 ± 0.3 [a] (p = 0.008) A significance level of 0.05 was applied as a cutoff value [a]Statistically significant results Overall, our results lead to a conclusion that altered expression of a particular SF may affect the levels of mirtronic miRNAs in the cell. [score:11]
Whereas a significant upregulation of SRSF2 -dependent expression was observed for hsa-miR-1227-3p (p = 0.008) and miR-1229-3p (p = 0.008), the hsa-miR-1226-3p did not exhibit statistically different (p = 0.15) expression levels between the HCT116 line and the line overexpressing the SRSF2 SF (Fig.   4b, the diagram at the right). [score:10]
It is currently shown that the mirtronic miRNA hsa-miR-1226-3p may function as an oncosuppressor by downregulating the mucin 1 oncoprotein and the hsa-miR-1226-3p level is decreased in breast cancer cells [19]. [score:6]
For example, hsa-miR-1226-3p processed from an artificial conventional mirtron effectively silences aberrant myotonic dystrophy protein kinase [35], mmu-miR-1224 leucine-rich repeat serine/threonine-protein kinase 2, and α-synuclein Parkinson disease -associated genes [36], while an artificial 3′-tailed mirtron knocks down the expression of the vascular endothelial growth factor A [34]. [score:6]
Compared with the healthy controls, the expression of hsa-miR-1226-3p was significantly higher in stomach tumors but extensively downregulated in colorectal tumors. [score:5]
SRSF1-specific and SRSF2-specific enhancers established nearby hsa-miR-1226-3p may point to the presence of a complex regulatory element with overlapping enhancer and silencer functions causing uneven expression levels of this miRNA in different biological repeats and high p values. [score:4]
Whereas steady levels of hsa-miR-1226-3p were detected in pancreatic cancer and healthy pancreatic tissues, two other mirtronic miRNAs, hsa-miR-1227-3p (p = 0.028) and hsa-miR-1236-3p (p = 0.017), were significantly downregulated in this tumor type. [score:4]
White vertical boxplots represent data from healthy tissues; gray from tumors Table 3 Expression of mirtronic miRNAs in colorectal, stomach, and pancreatic cancerous tissues compared to healthy tissues Cancerous tissue miRNAs of mirtron origin Non-mirtronic miRNA miR-1226-3p miR-1227-3p miR-1229-3p miR-1236-3p miR-1238-3p Colorectal − No change No change No change No change Stomach + No change No change No change No change Pancreatic No change − No change − No changeData were considered significant for p < 0.05 − reduced expression compared to the non-cancerous tissue, + increased expression Despite a considerable progress in the study of biogenesis of mirtron-derived miRNAs, the factors responsible for mirtronic intron splicing are not known. [score:4]
Dendrogram of hierarchy clustering analysis is presented at the left Table 2 Differential expression of mirtronic miRNAs in pancreas, kidney, colon, and stomach cancer cell lines Organ Cell line miRNAs of mirtron origin Non-mirtronic miRNA miR-1226-3p miR-1227-3p miR-1229-3p miR-1236-3p miR-1238-3p Pancreas PANC-1−2.8 ± 1.8 [a] −1.7 ± 0.3 [a] −2.8 ± 0.9 [a] −1.4 ± 0.2 −1.2 ± 0.6 SU. [score:3]
The expression levels of hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p dramatically decreased and comprised less than 5 % of the levels observed for the WT minigenes (Table  1). [score:3]
Concomitant evaluation of the miRNA expression levels by RT-qPCR showed a statistically significant increase of hsa-miR-1229-3p but not hsa-miR-1226-3p or hsa-miR-1227-3p in response to SRSF1 overexpression (Fig.   4b, the diagram at the left, and Table  4). [score:3]
We found that only one out of five tested miRNAs, hsa-miR-1226-3p, was significantly under-expressed in the colorectal tumor (p < 0.001). [score:3]
86.86, T3M4, stomach KATOIII, colon HCT116) or the excretory system (kidney CaKi-1, 786-O) were chosen to define whether the expression of the human mirtronic miRNAs hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p and canonical hsa-miR-1238-3p varies between the cancerous cells. [score:3]
Digestive and excretory system cancer cell lines, as well as digestive system tumors tissues, display varying expression profiles of the previously identified hsa-miR-1226-3p and the two newly validated mirtronic miRNAs. [score:3]
Despite the fact that the first splicing -dependent human mirtrons were annotated in 2007 [15] and a large number of splicing-derived miRNAs have been predicted by bioinformatic analysis of deep sequencing data [12, 14], only two of them, hsa-miR-877-5p and hsa-miR-1226-3p, were experimentally proven to be directly affected by splicing [16, 17]. [score:2]
The miRNA variability in cancer cell lines was determined by changes in abundance of two mirtronic miRNAs, hsa-miR-1229-3p and hsa-miR-1236-3p, while the expression levels of hsa-miR-1226-3p and hsa-miR-1227-3p declined in all tested cancer cell lines compared to those in HEK 293A. [score:2]
Schemes represent protein-coding genes, harboring reside-verified mirtronic miRNA hsa-miR-1226-3p, putative conventional mirtronic miRNAs hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1238-3p, mirtronic miRNAs, located in 5′-tailed mirtrons hsa-miR-3064-5p and hsa-miR-6515-5p and mirtronic miRNAs, located in 3′-tailed mirtrons hsa-miR-3940-5p and hsa-miR-6850-5p. [score:1]
The vast majority of nearly 500 mirtron-derived miRNA candidates, except hsa-miR-887 and hsa-miR-1226-3p processed from conventional mirtrons, are still listed as experimentally unverified [14, 16, 17]. [score:1]
The abundance of two of them, hsa-miR-1226-3p and hsa-miR-1227-3p, was reduced two- to five-fold in all cancer cell lines relative to the embryonic kidney HEK 293A cells. [score:1]
Previous studies demonstrated that cellular levels of hsa-miR-1226-3p and hsa-miR-1236-3p inversely correlate with cancerogenesis in breast and hepatoma cancer cells, respectively [20, 33]. [score:1]
The levels of hsa-miR-1226-3p decreased in the T3 stage colorectal but conversely increased in the stomach cancer tissues. [score:1]
In this study, cell line-specific profiles of miRNAs processed from conventional mirtrons, hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p, in seven various pancreatic, kidney, colorectal, and stomach cancer cell lines were identified (Table  2). [score:1]
Nevertheless, their dependence on splicing was experimentally validated only for two human miRNAs located in conventional mirtrons, hsa-miR-877-5p and hsa-miR-1226-3p [16, 17]. [score:1]
These results convincingly confirmed that the biogenesis of hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p is strictly splicing -dependent, thus the efficiency of the splicing machinery defines the quantity of these miRNAs. [score:1]
Introns containing validated mirtronic miRNA hsa-mir-1226-3p or predicted miRNAs hsa-mir-1227-3p, hsa-mir-1229-3p, hsa-mir-1236-3p, and hsa-mir-1238-3p processed from conventional; hsa-miR-3064-5p and hsa-miR-6515-5p from 5′-tailed; and hsa-miR-3940-5p and hsa-miR-6850-5p from 3′-tailed mirtrons are depicted as red lines. [score:1]
A plasmid with the MG1226/DHX30 minigene containing the functionally proven mirtronic hsa-miR-1226-3p [16] was used as a positive control. [score:1]
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For instance, hsa-miR-1226-3p, hsa-miR-23b-5p, hsa-let-7d-5p, and hsa-miR-30c-5p, which were initially identified as increasing in expression in response to F. tularensis exposure by RNAseq, were also found to increase in expression after exposure to E. coli or B. pseudomallei, although in the case of E. coli and B. pseudomallei exposure, this increase was detected by qPCR and not by RNAseq. [score:5]
These 4 miRNAs are, in ascending P value order, hsa-miR-1226-3p (P = 0.0113), hsa-miR-23b-5p (P = 0.0136), hsa-let-7d-5p (P = 0.0175), and hsa-miR-30c-5p (P = 0.02408). [score:1]
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SNPID Position in 3′UTR Polymorphism Predicted microRNA Seed region Number of raw reads Ts10059 18 C/T hsa-miR-31 Y 0 Ts41266889 196 C/T hsa-miR-3153 Y 0 Ts180769907 360 A/T hsa-miR-1226* Y 0 hsa-miR-608 N 0 hsa-miR-92a* N 0 Ts1043230 367 C/A hsa-miR-92a-2* Y 0 hsa-miR-4298 N 0 Ts1043329 460 C/T hsa-miR-24 N 150 Ts141849450 515–516 delCA hsa-miR-455-5p Y 95 Ts34629439 582 delT hsa-miR-1301 N 45 hsa-miR-590-5p N 11 hsa-miR-27b* N 23 hsa-miR-582-5p N 15 hsa-miR-656 N 107 Ts113810300 623 T/G hsa-miR-1252 Y 0 hsa-miR-3125 Y 0 hsa-miR-340 Y 1708 hsa-miR-142-5p Y 20 hsa-miR-186 Y 1209 hsa-miR-3121 N 0 hsa-miR-4311 N 0 Ts71719087 638/639 delAT hsa-miR-3145 Y 0The SNP ID and the nature of the polymorphism are indicated. [score:1]
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Finally, we synthesized the miRNA mimic for miR-1226 and found that it affected growth of E. coli in vitro and when given orally to mice also affected E. coli in vivo. [score:1]
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[+] score: 1
Mutant alleles T and A create the interactions between MEFV mRNA and miR-1226/4252/4733-3p as well as MEFV mRNA miR-4435/4645-5p/4673. [score:1]
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