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57 publications mentioning hsa-mir-216b

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-216b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 184
Approach to identifying miR-216b-3p target genes by in silico analysis of genome-wide gene expression, TargetScan and GEO database analysis of miR-216b-3p transfectants and PDAC clinical specimens. [score:7]
Genome-wide gene expression and in silico analysesTo identify miR-216b-3p target genes, a combination of genome-wide gene expression and in silico analyses was conducted as described previously [20, 28, 51, 52]. [score:7]
The expression of FOXQ1 was directly regulated by miR-216b-3p and its overexpression was involved in PDAC pathogenesis. [score:7]
In gene expression analyses, 439 and 806 genes were downregulated (log [2] ratio <-1.0) in PANC-1 and SW 1990 miR-216b-3p transfectants, respectively, in comparison with control transfectants (GEO accession number, GSE82108). [score:6]
FOXQ1 is a direct target of miR-216b-3p in PDAC cellsWe performed qRT-PCR to validate miR-216b-3p -mediated reduction of FOXQ1 mRNA expression in PDAC cell lines. [score:6]
Wild-type sequences of the 3 [׳]-UTR of FOXQ1 containing the 2 miR-216b-3p target sites (positions 463-468 or 720-727) sequences or lacking a miR-216b-3p target site were inserted in the psiCHECK-2 vector (product ID: C8021; Promega, Madison, WI, USA). [score:5]
To identify miR-216b-3p target genes, a combination of genome-wide gene expression and in silico analyses was conducted as described previously [20, 28, 51, 52]. [score:5]
Negative correlations between miR-216b-3p expression and FOXQ1 mRNA expression were found using Spearman’s rank test (R = -0.5160, P = 0.0006, Figure 5B). [score:5]
In this study, FOXQ1 (a member of the forkhead transcription factor family) was identified as a direct target of miR-216b-3p regulation in PDAC cells. [score:5]
Figure 2Expression levels of miR-216 family membersExpression levels of miR-216 family members in clinical specimens and PDAC cell lines were determined using qRT-PCR. [score:5]
Identification of genes regulated by miR-216b-3p in PDAC cellsTo elucidate the molecular mechanisms and pathways regulated by anti-tumour miR-216b-3p in PDAC cells, we used a combination of gene expression and in silico analyses. [score:5]
Transcription of all members of the miR-216 cluster was significantly reduced in PDAC specimens, and ectopic expression of these miRNAs suppressed cancer cell aggressiveness. [score:5]
To better understand and identify the anti-tumour targets of miR-216b-3p in PDAC cells, we have applied in silico database and genome-wide gene expression analyses. [score:5]
Figure 4Flow chart illustrating the analytic strategy for miR-216b-3p target genesStrategy for identification of putative candidate genes regulated by miR-216b-3p in PDAC cells. [score:4]
Candidate target genes regulated by miR-216b-3p in PDAC. [score:4]
FOXQ1 is a direct target of miR-216b-3p in PDAC cells. [score:4]
In conclusion, downregulation of 4 clustered miRNAs (miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p) was detected by RNA sequencing -based miRNA signature analysis. [score:4]
To elucidate the molecular mechanisms and pathways regulated by anti-tumour miR-216b-3p in PDAC cells, we used a combination of gene expression and in silico analyses. [score:4]
Expression levels of the miR-216 family in PDAC specimens and cell lines. [score:3]
Among the miR-216 family, miR-216b-3p markedly inhibited PDAC cell aggressiveness (Figure 3). [score:3]
To elucidate molecular mechanisms of low expression of the clustered miRNAs, miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p in PDAC cells, PANC-1 and SW1990 cells were treated with the demethylating agent [5-aza-2’-deoxycytidine (5-aza-dC)]. [score:3]
Expression of miR-216-3p levels were significantly higher than those of mock and miRNA control transfected cells (Supplementary Figure 2). [score:3]
Patient clinicopathological features are summarized in Table 1. The expression levels of miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p were significantly lower in tumour tissues than in normal pancreatic tissues (Figure 2). [score:3]
We found that 20 genes were putatively targeted by miR-216b-3p in PANC-1 and SW 1990 miR-216b-3p transfectants. [score:3]
Expression levels of the miR-216 family in PDAC specimens and cell linesWe evaluated expression levels of the miR-216 family in PDAC tissues (n = 24), normal pancreatic tissues (n = 14) and two PDAC cell lines (PANC-1 and SW 1990). [score:3]
We performed qRT-PCR to validate miR-216b-3p -mediated reduction of FOXQ1 mRNA expression in PDAC cell lines. [score:3]
Moreover, expression levels of miR-216a-5p, miR-216a-3p and miR-216b-5p were same levels of mock and miRNA control transfectants (Supplementary Figure 2). [score:3]
It was not recognized the significant relationships between any of the clinical parameters (i. e., TNM stage, metastasis or survival rate) and expression levels of any member of the miR-216 -family (data not shown). [score:3]
Direct regulation of FOXQ1 by miR-216b-3p in PDAC cells. [score:3]
Expression levels of miR-216 family members in clinical specimens and PDAC cell lines were determined using qRT-PCR. [score:3]
Expression levels of miR-216 family members. [score:3]
In that study, 3 miRNAs (miR-216a, miR-216b, and miR-217) were reduced in expression in the Kras [G12D] pancreas. [score:3]
Flow chart illustrating the analytic strategy for miR-216b-3p target genes. [score:3]
FOXQ1 protein expression was also repressed in the miR-216b-3p transfectants (Figure 6B). [score:3]
Expression of miR-216 family members and the effects on cell growth, migration and invasion in PDAC cell lines. [score:3]
Figure 4 presents the strategy for narrowing down the target genes of miR-216b-3p. [score:3]
Figure 6Direct regulation of FOXQ1 by miR-216b-3p in PDAC cells (A) FOXQ1 mRNA expression was evaluated using qRT-PCR in PANC-1 and SW 1990 cells 72 h after transfection with miR-216b-3p. [score:3]
Expression of miR-216 family members and the effects on cell growth, migration and invasion in PDAC cell linesThe functional roles of the miR-216 -family were performed by using restoration of mature miRNAs assays. [score:2]
Dual luciferase reporter assays using vectors encoding putative miR-216b-3p target sites of the FOXQ1 3’-UTR (positions 463-468 and 720-727) for both wild-type and deleted regions. [score:2]
Compared with the miR-control, luminescence intensity was significantly reduced by transfection with miR-216b-3p at its target site, position 720-727 in the 3’-UTR of FOXQ1 (Figure 6C). [score:2]
Strategy for identification of putative candidate genes regulated by miR-216b-3p in PDAC cells. [score:2]
Identification of genes regulated by miR-216b-3p in PDAC cells. [score:2]
Among them, we focused on 4 clustered miRNAs, miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p located on human chromosome 2p16.1. [score:1]
Functional assays showed that proliferation, migration and invasion activities of cancer cells were significantly suppressed in miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p transfectants compared with mock or miR-control transfectants (Figure 3). [score:1]
Effects of miR-216a-5p, miR-216a-3p, miR-216b-5p and miR-216b-3p transfection into PDAC cells. [score:1]
Present results suggested that the miR-216 family could have anti-tumour functions in PDAC cells. [score:1]
Schematic representation of the human miR-216 family in chromosomal location. [score:1]
Pre-miR [™] miRNA precursors for miR-216a-5p (product ID: PM10545; Thermo Fisher Scientific), miR-216a-3p (product ID: PM24316), miR-216b-5p (product ID: PM12302), miR-216b-3p (product ID: PM28358), negative control miRNA (product ID: AM 17111), two FOXQ1 siRNAs (product IDs: s41290 and s41291) and control siRNA (product ID: D-001810-10) were purchased from Thermo Fisher Scientific. [score:1]
Likewise pre- miR-216a, miR-216b-5p (guide strand) and miR-216b-3p (passenger strand) are derived from pre- miR-216b. [score:1]
Because the role of the miR-216 cluster had not been reported in PDAC, we focused on it in further studies. [score:1]
Past studies showed that guide strands of miR-216a-5p and miR-216b-5p acted as anti-tumour miRNAs in several cancers [29, 30]. [score:1]
Here, we showed that the clustered miR-216 family has anti-tumour activity in PDAC. [score:1]
Those results suggest that the miR-216 family is important in PDAC oncogenesis. [score:1]
The miR-216 family members and miR-217 are located on human chromosome 2q16.1. [score:1]
On the other hand, the functional significance of passenger strands miR-216a-3p and miR-216b-3p has not been adequately analysed. [score:1]
Seed sequences of miR-216a-5p and miR-216b-5p are identical. [score:1]
We found that miR-217, miR-216a-5p/-3p and miR216b-5p/-3p were close together and were defined as clustered miRNAs. [score:1]
We hypothesized that passenger strand of miR-216-3p may be incorporated into and function as part of the RISC structure. [score:1]
Nevertheless, our present data showed that passenger strands miR-216a-3p and miR-216b-3p have anti-tumour functions in PDAC cells. [score:1]
This miRNA is located in the same genomic region as the miR-216 cluster. [score:1]
We further investigated the target genes of miR-216. [score:1]
The correlation between the expression levels of miR-216b-3p and FOXQ1 was evaluated using Spearman's rank test. [score:1]
In contrast, seed sequences of miR-216a-3p and miR-216b-3p are independent sequences. [score:1]
We evaluated expression levels of the miR-216 family in PDAC tissues (n = 24), normal pancreatic tissues (n = 14) and two PDAC cell lines (PANC-1 and SW 1990). [score:1]
After transfection with miR-216-3p, Ago2-bound miRNAs were isolated, and RT-qPCR was carried out to determine whether miR-216-3p bound to Ago2. [score:1]
As shown in Figure 1, miR-216a-5p/-3p and miR216b-5p/-3p are located within the same chromosomal region (2q16.1). [score:1]
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2
[+] score: 96
Our in silico analysis revealed that miR-216 and miR-217 potentially target many important genes that play critical roles during the pathogenesis of PC (Table 1); and the downregulation of miR-217 [45] and miR-216 [44] suggests their potential as tumor suppressors in PC by targeting downstream targets, particularly the Kras oncogene [43] and Janus kinase 2 [44]. [score:12]
At 30 weeks of age, the expression of miR-216 (p-value = 0.016), miR-217 (p-value = 0.0078), miR-150 (p-value =0.023), Let-7b (p-value = 0.031,) and miR-96 were significantly downregulated, whereas the expression of miR-146b (p-value = 0.0078), miR-205, (p-value - 0.0078), miR-21, miR-195 (p-value = 0.031), and miR-34c (p-value = 0.063) were significantly upregulated in KC animals compared to control animals (Figure 2B). [score:10]
The expression of miR-223, miR-483-3p (p-value = 0.01), 146b, 205 (p-value = 0.001), 221, 21 (p-value = 0.023), 195, 34c and miR-26a (p-value = 0.0078) were significantly upregulated, whereas the expression of miR-216, miR-141, miR-217, Let-7b (p-value = 0.001), and Let-150 (p-value = 0.01) were significantly downregulated in human PC tissues as compared to the cancer-adjacent normal tissues (Figure 3E). [score:10]
At 40 weeks of age, the expression of miR-216, miR-217, miR-223, miR-141, miR-483-3p (p-value = 0.031), miR-195, Let-7b (p-value = 0.063) and miR-96 were significantly downregulated; on the other hand, the expression of miR-21, miR-205, miR-146b (p-value = 0.031), and miR-34c (p-value = 0.063) were upregulated in KC mice compared to the control animals (Figure 2C). [score:10]
The panel of differentially expressed miRNAs were validated by real-time PCR using TaqMan assays, and the results were consistent with the data that showed up-regulation of miR-21, miR-221, miR-100 and miR-26a and down-regulation of miR-26b, miR-141, miR-96, miR483-3p, miR-216, and miR-217 in the KC compared to control mice (Figure 1A). [score:7]
In addition to KC mice, we also observed a significant downregulation of miR-216 and miR-217 in human PC tissue (Figure 3E); these results are in agreement with earlier studies on human PC [38– 43] that show downregulation of miR-217 in 76.2% (16/21) of PC tissue as well as cell lines [43]. [score:7]
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
Similarly, the expression of miR-216 is significantly downregulated in PC [44]. [score:6]
Several studies have shown the abnormal expression of miRNAs including miR-21, Let-7b, miR-100, miR-217, and miR-216 in PC and have proposed them as candidates for early diagnosis and potential molecular targets [23, 24]. [score:5]
The expressions of miR-216 and miR-217 were also progressively reduced in KC mice, but the expressions of miR-21, miR-205, miR-146b, miR-34c, and miR-223 progressively increased (Figure 1A, 2A– 2D). [score:5]
The expression of pancreas-specific tumor suppressors miR-217 and miR-216 were unaltered at 10 weeks of age (presence of PanIN-Ia and Ib), but progressively decreased from 25 – 50 weeks of age as PanIN lesions progressed to PDAC. [score:5]
Both miR-216 and miR-217 act as potential tumor suppressors for PC by targeting the Kras oncogene [43]. [score:5]
Further, at 50 weeks of age, the expression of miR-216, miR-217, miR-345, miR-141, miR-483-3p, miR-26b, miR-96, Let-7b (p-value = 0.01), miR-100, miR-26a and miR-150 (p-value = 0.094) were further downregulated in KC animals compared to control mice (Figure 2D). [score:5]
On the other hand, miR-146b, miR-34c, miR-223, miR-195 (p-value = 0.031) and miR-216 (p-value = 0.063) were downregulated in KC mice compared to control littermates. [score:3]
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3
[+] score: 62
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-216a
Results revealed that patients with lymph node metastasis showed significantly lower miRNA-216b expression level than patients without lymph node metastasis (0.068 ± 0.054 versus 0.134 ± 0.117, P = 0.0168) (Figure 3(b)), while the miRNA-216a expression level showed no significant difference (P = 0.0845) (Figure 3(a)); patients with TNM IV showed significantly lower miRNA-216a expression level than patients with TNM 0-I or TNM II (0.039 ± 0.022 versus 0.088 ± 0.062, P < 0.05; 0.039 ± 0.022 versus 0.086 ± 0.065, P < 0.05) (Figure 3(c)); and patients with TNM III showed significantly lower miRNA-216b expression level than patients with TNM 0-I (0.072 ± 0.067 versus 0.134 ± 0.119, P < 0.05) (Figure 3(d)). [score:9]
Deng et al. [21] found that miRNA-216b was downregulated in NPC cell lines and specimens and played a tumor suppressive role in NPC by targeting KRAS. [score:8]
In HCC, miRNA-216b could function as a tumor suppressor by targeting IGF2BP2 and subsequently suppressing the downstream IGF2 [22]. [score:7]
Among the 21 patients who underwent esophagectomy, the number (proportion) of patients with upregulated miRNA-216b expression after esophagectomy was 19 (90.5%), while the number (proportion) was only 14 (66.7%) for miRNA-216a. [score:6]
We found that the expression level of plasma miRNA-216b in postoperative samples was significantly upregulated compared with that of preoperative samples (0.132 ± 0.037 versus 0.088 ± 0.051, P = 0.0074) (Figure 2(b)). [score:5]
In cooperation with other three miRNAs, miRNA-216b could induce cellular senescence through the p53-p21 [Cip1/WAF1] pathway by protein kinase CKII downregulation -mediated ROS production in human colorectal cancer cells [31]. [score:4]
What is more, we found that the expression level of plasma miRNA-216b after esophagectomy was significantly upregulated, thus providing a useful insight into the application of plasma miRNA-216b in the evaluation of therapeutic effect. [score:4]
miRNA-216b was downregulated in nasopharyngeal carcinoma (NPC) [21] and HCC [22]. [score:4]
In HCC, plasma miRNA-216b was revealed to be significantly downregulated compared with healthy volunteers [22]. [score:3]
As a homologous miRNA of miRNA-216b, theoretically, miRNA-216a is expected to exhibit similar expression after esophagectomy. [score:3]
Recently, miRNA-216a/b, as two members of miRNA-216 family, have been demonstrated to be dysregulated in several types of human cancers. [score:2]
miRNA-216a/b, two members of miRNA-216 family, have been demonstrated to be dysregulated in several types of human cancers. [score:2]
At the cut-off value of 0.070, the sensitivity was 80.0% and the specificity was 90.2% for miRNA-216a; and at the cut-off value of 0.060, the sensitivity was 55.8% and the specificity was 90.2% for miRNA-216b. [score:1]
Plasma miRNA-216a was superior to miRNA-216b in the diagnosis of ESCC (z = 3.141; P = 0.0017) (Figure 4). [score:1]
We found that plasma miRNA-216a/b could differentiate ESCC patients from healthy controls, with an AUC of 0.877 (95% CI: 0.818–0.922) for miRNA-216a and 0.756 (95% CI: 0.685–0.819) for miRNA-216b, respectively. [score:1]
Therefore, it might be the small sample size that resulted in the inconformity between miRNA-216a and miRNA-216b. [score:1]
ROC curve analysis showed that plasma miRNA-216a/b exhibited satisfactory diagnostic value for ESCC, with AUC of 0.877 (95% CI: 0.818–0.922) for miRNA-216a and 0.756 (95% CI: 0.685–0.819) for miRNA-216b, which were higher than conventional biomarkers such as SCC-Ag (AUC: 0.665) and CEA (AUC: 0.549) reported in other studies [13, 16]. [score:1]
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4
[+] score: 14
RT-PCR validated three significantly upregulated miRNAs and three significantly downregulated miRNAs namely miR-217, miR-216a, miR-216b, miR-146a, miR-509-3p and miR-211. [score:7]
For validation using RT-PCR, we chose three miRNAs (miR-217, miR-216a, and miR-216b) that were upregulated and three miRNAs (miR-146a, miR-509-3p, miR-211) that were downregulated by at least 6 standard deviations in tumor compared to control arrays. [score:6]
Both miR-216a and miR-216b are associated with various types of cancer in particular adenocarcinoma of the pancreas. [score:1]
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5
[+] score: 13
Other miRNAs from this paper: hsa-mir-216a, hsa-mir-126
Simultaneously, αvβ1, FAK, and p38 siRNA reversed OBCM -inhibited miR-126 expression and promoter activity (Fig. 5E–F), indicating that osteoblast-derived WISP-1 suppresses miR-216 via the αvβ1/FAK/p38 pathway. [score:7]
Taken together, these data demonstrate that miR-216 directly represses VCAM-1 protein expression via binding to the 3′UTR of human VCAM-1 through the αvβ1/FAK/p38 signaling pathway. [score:4]
To examine whether miR-216 regulates the 3′UTR of VCAM-1, we constructed a luciferase-reporter vector harboring the 3′UTR of VCAM-1 mRNA and another vector containing the miR-216 -binding site. [score:2]
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6
[+] score: 13
The lncRNA urothelial carcinoma -associated 1 (UCA1) was shown to work as an endogenous sponge that can down-regulate miR-216b expression by directly binding to miR-216b (Wang et al., 2015). [score:7]
Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway. [score:6]
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7
[+] score: 11
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Ssc-miR-216 and ssc-miR-217 were also located in the same genome loci in chromosome 3. Overexpression of has-miR-216a/217 activates the PI3K/Akt and TGF-β signaling pathways by targeting PTEN and SMAD7 in human hepatocellular carcinoma cells [54]. [score:5]
Additionally, ssc-miR-216, ssc-miR-217, ssc-miR-142-5p, ssc-miR-96-5p, ssc-miR-182 and ssc-miR-183 have higher expression levels in mpiPSCs than that in hpiPSCs (Fig 3A). [score:3]
Ssc-miR-216 was also highly expressed in mpiPSCs. [score:3]
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8
[+] score: 11
Other tissue-specific miRNAs identified by our analysis that were also reported to be tissue-specific in other species include: miR-122, a liver-specific miRNA that functions as a tumor-suppressor gene in hepatocellular carcinoma [29]; miR-216, a pancreas-enriched miRNA, which has been reported as a marker for acute phase pancreatic injury and whose down-regulation is thought to be crucial in the development of pancreatic cancer [30]; miR-150, which our analysis reported as enriched in lymph nodes, is known to be expressed in mature B and T cells and, in particular, to regulate differentiation and the cytolytic effector function in CD8+ T cells [31]. [score:10]
Endo K Weng H Kito N Fukushima Y Iwai N MiR-216a and miR-216b as markers for acute phased pancreatic injuryBiomed. [score:1]
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9
[+] score: 10
Therefore, miRNAs up-regulated in F50 cerebellum (e. g. miR-135a, miR-135b and miR-7, see Figure 2) and F100 cerebellum (e. g. miR-216a and miR-216) make promising candidates for developmental switches in the cerebellum. [score:5]
An interesting expression pattern is represented by miR-216a, miR-216b and miR-217 which were found to be exclusively expressed in the F100 cerebellum, implying that they are highly stage- and tissue-specific miRNAs. [score:5]
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10
[+] score: 10
Other miRNAs from this paper: hsa-mir-211
For example, the miR-216b is proved to be a direct target of CHOP and thereby executes its pro-apoptotic activity by suppression of c-Jun expression (83). [score:8]
miR-216b regulation of c-Jun mediates GADD153/CHOP -dependent apoptosis. [score:2]
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11
[+] score: 8
UCA1 is thought to contribute to HCC development/pathogenesis by acting as an endogenous sponge that directly binds to miR-216b and downregulates miR-216b expression (Figure 1). [score:8]
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[+] score: 8
Multiple LncRNAs are demonstrated to be correlated to HCC, Wang et al. [20] indicated that LncRNA-UCA1 up-regulation promotes HCC progression accompanied by miR-216b inhibition, and Lv et al. showed that LncRNA H19 and miR-675 inhibition contributes to migration and invasion of HCC [21]. [score:8]
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13
[+] score: 8
Wang F Ying HQ He BS Pan YQ Deng QW Sun HL Chen J Liu X Wang SK Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathwayOncotarget. [score:8]
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14
[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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15
[+] score: 7
In addition, miR-216b suppresses the proliferation and invasion via inhibiting KRAS expression [19]. [score:7]
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16
[+] score: 7
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-365a, 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-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
For example, miR-142-5p and miR-142-3p (hematopoietic system), miR-122 (liver), and miR-216 and miR-217 (pancreas) were highly expressed in these organs and less abundantly in HM [48, 177], suggesting that these HM microRNAs may originate from the maternal bloodstream to specifically target the development, growth and function of the corresponding organs in the HM fed infant. [score:6]
These include for example muscle miR-1 and miR-133 [173], brain miR-9 and miR-124a [178], pancreatic miR-216 and miR-217 [179], liver miR-122 [21, 173], blood cell miR-451 [180], and endothelial cell miR-126 [181]. [score:1]
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17
[+] score: 7
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-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, 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-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, 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-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, 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-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, 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-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, 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, hsa-mir-486-2
When globally analyzed the relapse-related miRNAs-miR-7, miR-100, miR-216 and let-7i—were up-regulated, and miR-486, miR-191, miR-150, miR-487 and miR-342 were down-regulated in early relapse ALL patients [76]. [score:7]
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18
[+] score: 7
Furthermore, miRNAs are subject to complex regulatory mechanisms so it is not surprising to observe numerous miRNAs with discordant copy number and expression (such as miR-216). [score:4]
Two miRNAs, miR-218 and miR-216, were common to training and all test sets, however, only miR-218 demonstrated concordant loss of copy number and expression (Figure 1). [score:3]
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19
[+] score: 7
RXRβ and TRβ, which initiated the process of metamorphosis, were up-regulated, while their predicted interaction miRNAs (mfi-miR-133c, mfi-miR-25, mfi-miR-31a and mfi-miR-363–3p; mfi-miR-15a, mfi-miR-15b and mfi-miR-216) were down-regulated. [score:7]
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20
[+] score: 7
MiR-216b decreased expression is directly related to aggressive nasopharyngeal carcinomas making this miRNA a potential prognosis biomarker [72]. [score:4]
MiR-216b was down-regulated in nasopharyngeal carcinoma and bound KRAS mRNA 3′-UTR. [score:3]
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21
[+] score: 6
Last hsa-miR-216 was upregulated in cancer patients as compared to patients diagnosed with pancreatitis, with sensitivity of 50% and specificity of 100%. [score:3]
We found that salivary hsa-miR-216 may help discriminate pancreatitis from PDAC, with excellent specificity (100%), but poor sensitivity (50%) (Table 3). [score:1]
In this pilot study, we found that four salivary miRNAs (hsa-miR-21, hsa-miR-23a, hsa-miR-23b and hsa-miR-29c) successfully segregated PDAC patients from cancer-free donors, while hsa-miR-210 and let-7c indicate pancreatitis and hsa-miR-216 discriminates pancreatitis from cancer. [score:1]
However, at this stage of this project, salivary testing failed to differentiate between pancreatitis and PDAC, as hsa-miR-216 is detected only in pancreatitis and not in cancer, but with poor sensitivity. [score:1]
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22
[+] score: 6
As a result, we identified the expression levels of five miRNAs, including let-7e, miR-204, miR-216b, miR-9, and miR-139-5p as significantly downregulated in the PVD group, as shown by lower -ΔCT values (Fig 1C and 1D). [score:6]
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23
[+] score: 6
MiR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells. [score:3]
For example, it is known that human miR-186-5p, miR-216b-5p, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting the gene CSNK2A1 in human colorectal cancer cells [35]. [score:3]
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24
[+] score: 6
Previous studies demonstrated that loss of some tumor suppressive miRNAs leads to PARP1 up-regulation in cancer, such as miR-216b, let-7, miR-345, and miR-221 [14–17]. [score:6]
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25
[+] score: 5
Pten, the inhibitor of PI3K/AKT, was targeted by miR-216 and miR-217 and these miRNAs were also activated by Tgfb1 [46]. [score:5]
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26
[+] score: 5
Lee et al reported that miR-122a is specifically expressed in liver tissue while miR-216 and miR-217 are preferentially expressed in the pancreas [38]. [score:5]
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27
[+] score: 4
Apparently, paclitaxel induces the autophagy through decreased miR-216b levels that normaly downregulate Beclin1 activation and causes autophagy activation in paclitaxel -treated cells resulting in a decreased paclitaxel -induced cell death due to the activation of autophagic cancer cell survival [165]. [score:4]
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28
[+] score: 4
Other miRNAs from this paper: hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-372
Upregulated UCA1 in HCC can promote progression through a novel UCA1-miR-216b-FGFR1-ERK signaling pathway [30]. [score:4]
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[+] score: 4
Serum was also analyzed by Q-RT-PCR for a panel of 20 tissue enriched and potential miRNA biomarkers, including those identified for liver (cfa-miR-122 and -885), heart/muscle (cfa-miR-1, -133, and -206), testis (miR-34b/c), pancreas (cfa-miR-216), brain (cfa-miR-212), and ubiquitously expressed cfa-miR-193b. [score:3]
A recent rat study demonstrated that plasma levels of miR-216a and miR-216b increased after pancreatic injury [34]. [score:1]
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[+] score: 4
There are at least two miR-216b binding sites in MALAT1 and the HIF-2α- MALAT1- miR-216b axis regulates multidrug resistance of HCC cells by modulating autophagy [146]. [score:2]
Yuan P. Cao W. Zang Q. Li G. Guo X. Fan J. The hif-2alpha-malat1-mir-216b axis regulates multi-drug resistance of hepatocellular carcinoma cells via modulating autophagyBiochem. [score:2]
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31
[+] score: 4
Conversely, 15 miRNAs resulted downregulated in activated B cells: mir-483, mir-95, mir-326, mir-135a, mir-184, mir-185, mir-516-3p, mir-30b, mir-203, mir-216, mir-150, mir-182*, mir-141 and mir-211 (Table 3). [score:4]
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[+] score: 4
MiR-216b-5p was increased in 1 vehicle treated animal and miR-217-5p was increased in 2 vehicle treated animals with no histopathologic or clinical chemistry correlates (data not shown). [score:1]
In 3 μg/kg treated dogs miR-216b-5p and miR-141-3p were increased at some time points, but miR-216b-5p was not increased beyond the level of the vehicle treated dog and did not display consistent time dependent increases. [score:1]
MiR-216b-5p reached levels as high as 649 fold above vehicle in individual animals and remained elevated until 24 h. The remaining miRNAs did increase and remained elevated generally as long, but not to the degree of miRs-216a-5p and 216b-5p. [score:1]
MiR-216b displayed similar kinetics to miR-216a-5p, but with a reduced dynamic range while miR-217-5p displayed increases similar to amylase. [score:1]
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[+] score: 3
[66] Moreover, MALAT1 can act as a 'sponge' for miR-216b to induce autophagy, probably through derepressing Beclin 1 expression, which, in consequence, ameliorates the multidrug resistance of HCC cells. [score:3]
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34
[+] score: 3
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-211, hsa-mir-299
LncRNA urothelial carcinoma -associated 1(lncRNA-UCA1) through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway in hepatocellular carcinoma [30]. [score:3]
[1 to 20 of 1 sentences]
35
[+] score: 3
For example, excessive CUDR contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway 34. [score:3]
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36
[+] score: 3
MiR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting alpha subunit of protein kinase CKII in human colorectal cancer cells. [score:3]
[1 to 20 of 1 sentences]
37
[+] score: 3
Regarding the role of UCA1 in HCC tumorigenesis, Wang et al. [19] found that UCA1 could facilitate HCC cell growth and metastasis through the inhibition of miR-216b and activation of the FGFR1/ERK signaling pathway. [score:3]
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38
[+] score: 3
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-142, hsa-mir-548c, hsa-mir-4668
There were also 12 differentially expressed precursor miRNA (Table 3), including hsa-mir-216b (FC = −2.09), hsa-mir-142 (FC = 2.20) and hsa-mir-548c (FC = 2.73). [score:3]
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39
[+] score: 3
Furthermore, the in silico analysis performed by Khongnomnan et al. predicted another 75 miRNAs that might target viral genes of IAV, including miR-216b, miR-3682, miR-4513, miR-4753 and miR-5693 [76]. [score:3]
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40
[+] score: 3
Previous studies have reported that miR-216a, miR-216b, and miR-217 are specifically expressed in the pancreas; these miRNAs were useful as biomarkers for pancreatic injury [30]. [score:3]
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41
[+] score: 3
miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells. [score:3]
[1 to 20 of 1 sentences]
42
[+] score: 2
Other miRNAs from this paper: hsa-mir-216a, mmu-mir-216a, mmu-mir-216b, mmu-mir-216c
Quantitative data suggested that the JAK2 expression in GC tissues with high miR-216 level was significantly decreased compared with those with low miR-216a level (P<0.05, Figure 5F). [score:2]
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43
[+] score: 2
By contrast, T- and B-cell regulatory miR-150 was not detected, and several tissue-specific miRNAs, such as miR-122 (liver), miR-216, miR-217 (pancreas) and miR-142-5p and miR-142-3p (hematopoietic cells), were barely detectable (Figure 1b). [score:2]
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44
[+] score: 2
Xu Z. Bu Y. Chitnis N. Koumenis C. Fuchs S. Y. Diehl J. A. miR-216b regulation of c-Jun mediates GADD153/CHOP -dependent apoptosisNat. [score:2]
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45
[+] score: 2
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-365a, 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-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
Ason et al. (2006) miR-7, miR-9, miR-34b, miR-96, miR-124a, miR-125b, miR-132, miR-181b, miR-182, miR-183, miR-184, and miR-204, miR-215, miR-216, miR-217 Zebrafish Microarray, ISH ? [score:1]
Soares et al. (2009) let-7a,b,c,f,i, miR-7b, miR-9-5p, miR-9-3p, miR-34b, miR-103, miR-107, miR-124a, miR-125a,b, miR-128, miR-129-3p, miR-132, miR-138, miR-181a,b, miR-216, miR-217, miR-219, and miR-375 Zebrafish Microarray, ISH ? [score:1]
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46
[+] score: 2
The miRNAs differentially regulated by prenatal stress includes miR-23a (up), miR-129-2 (up), miR-361 (down), let-7f (up), miR-17-5p (down), miR-98 (up), miR-425 (down), miR-345-5p (down), miR-9 (up), miR216-5p (up), miR-667 (up), and miR-505 (down) (Figure 3A). [score:2]
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47
[+] score: 2
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-21, hsa-mir-22, hsa-mir-25, hsa-mir-33a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-141, mmu-mir-155, mmu-mir-10b, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-183, mmu-mir-184, hsa-mir-192, mmu-mir-200b, hsa-mir-129-1, mmu-mir-122, 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-183, hsa-mir-210, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-129-2, hsa-mir-184, mmu-mir-192, 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-21a, mmu-mir-22, mmu-mir-96, mmu-mir-34a, mmu-mir-129-2, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-25, mmu-mir-210, mmu-mir-181a-1, mmu-mir-216a, mmu-mir-223, mmu-mir-33, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, mmu-mir-217, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-375, mmu-mir-375, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-33b, mmu-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, mmu-mir-216c, bbe-let-7a-1, bbe-let-7a-2, bbe-mir-10a, bbe-mir-10b, bbe-mir-10c, bbe-mir-125a, bbe-mir-125b, bbe-mir-129a, bbe-mir-129b, bbe-mir-133, bbe-mir-1, bbe-mir-183, bbe-mir-184, bbe-mir-200a, bbe-mir-200b, bbe-mir-210, bbe-mir-216, bbe-mir-217, bbe-mir-22, bbe-mir-252a, bbe-mir-252b, bbe-mir-278, bbe-mir-281, bbe-mir-33-1, bbe-mir-33-2, bbe-mir-34a, bbe-mir-34b, bbe-mir-34c, bbe-mir-34d, bbe-mir-34f, bbe-mir-375, bbe-mir-7, bbe-mir-71, bbe-mir-9, bbe-mir-96, bbe-mir-34g, bbe-mir-34h, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In contrast, many phylogenetically conserved miRNAs, as well as miRNAs present in both chordates and vertebrates (for example, miR-216, miR-217, miR-22, miR-25, and miR-96), could be reliably traced back to B. belcheri (Gray). [score:1]
Based on the available nematode, fruitfly, zebrafish, frog, chicken, mouse, rat and human miRNA information [18], 45 conserved amphioxus miRNAs could be classified into three distinct groups: 23 miRNAs (let-7a, miR-1, miR-7, miR-9, and so on) were conserved throughout the Bilateria; 5 miRNAs (miR-252a, miR-252b, miR-278, miR-281 and miR-71) were homologous to invertebrate miRNAs; and 17 miRNAs (miR-141, miR-200a, miR-200b, miR-183, miR-216, miR-217, miR-25, miR-22, miR-96, and so on) were present both in chordates and vertebrates (Table S9 in). [score:1]
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48
[+] score: 2
Previous study reported that miR-216 and miR-217 promoted TGF β -induced MC hypertrophy in vitro by regulating PTEN 32. [score:2]
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49
[+] score: 1
, miR-194, miR-207, miR-107 [13], miR-215, miR-192 14, 15 miR-16-1, miR-143, miR-145, and miR-216 [9]. [score:1]
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50
[+] score: 1
Each poly-miRTS was either found in several alleles (e. g. miR-224 site in SLA-3), or in a single allele (e. g. miR-216 site in SLA-3: gb_EU432082.1 allele) (e. g. SLA-3: Figure 2). [score:1]
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51
[+] score: 1
07] 0.01 1p36.33 hsa-miR-126 −0.36 [−0.64 – −0.08] 0.01 9q34.3 hsa-miR-888 −0.56 [−1.02 – −0.10] 0.02 Xq27.3 hsa-miR-517b −0.22 [−0.41 – −0.03] 0.03 19q13.42 hsa-miR-363 −0.43 [−0.80 – −0.05] 0.03 Xq26.2 hsa-miR-216b −0.26 [−0.50 – −0.03] 0.03 2p16.1 hsa-miR-1285 −0.27 [−0.53 – −0.02] 0.04 7q21. [score:1]
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52
[+] score: 1
The elements were predicted to bind the annotated miRNAs called MIR45, MIR166 and MIR216 [32]. [score:1]
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53
[+] score: 1
Liu FY MiR-216b is involved in pathogenesis and progression of hepatocellular carcinoma through HBx-miR-216b-IGF2BP2 signaling pathwayCell Death Dis. [score:1]
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54
[+] score: 1
Furthermore, many miRNAs* (e. g., miR-20a* and miR-216b*) were sequenced at similar frequencies to their corresponding mature miRNAs (miR-20a and miR-216b). [score:1]
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55
[+] score: 1
Other miRNAs from this paper: hsa-mir-107, hsa-mir-331
Lee et al. [26] suggested that miR-216b affects HCC growth and metastasis through the FGFR1/ERK signaling pathway. [score:1]
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56
[+] score: 1
However, between LDM and PMM, there were only five miRNAs that exhibited different methylation levels in their promoter regions, including miR-378, miR-181c, miR-181d, miR-139 and miR-216 (Supplementary Table S5). [score:1]
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57
[+] score: 1
Cir-ITCH has been verified to bind with many different miRs, including, miR-7, miR-17, miR-214, miR-128, and miR-216b [2, 14, 55]. [score:1]
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