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24 publications mentioning mmu-mir-216a

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

1
[+] score: 283
Other miRNAs from this paper: hsa-mir-216a, mmu-mir-216b, hsa-mir-216b, mmu-mir-216c
Our data showed that JAK2 expression was obviously downregulated by miR-216a overexpression in both MGC-803 and BGC-823 cells (P<0.05, respectively, Figure 5B and 5C). [score:8]
Notably, miR-216a overexpression reduced the expression of phosphorylated STAT3 and its downstream targets including Slug, Snail and Twist in MGC-803 cells (P<0.05, respectively, Figure 6). [score:7]
Previous study reports that miR-216a expression is upregulated by by the androgen pathway in a ligand -dependent manner in HCC [18]. [score:6]
org/10.3390/ijms17060945 10 Zhang J Xu K Shi L Zhang L Zhao Z Xu H Liang F Li H Zhao Y Xu X Tian Y Overexpression of MicroRNA-216a suppresses proliferation, migration, and invasion of glioma cells by targeting leucine-rich repeat-containing G protein-coupled receptor 5Oncol Res 2017 https://doi. [score:6]
miR-216a expression is downregulated in GC tissues and cells. [score:6]
miR-216a inhibits migration, invasion and EMT process of GC cells probably by inhibiting activation of JAK2/STAT3 pathway. [score:5]
miR-216a inhibited migration, invasion and EMT process of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
miR-216a suppresses invasion, migration and proliferation of glioma cells by inhibiting leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5)[10]. [score:5]
miR-216a inhibits migration and invasion of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
Our results demonstrated miR-216a inversely modulated activation of JAK2/STAT3 pathway and the expressions of its downstream targets including Slug, Snail and Twist in GC cells. [score:5]
Thus, predicting and confirming the targets of miR-216a are important to disclose the molecular mechanisms by which miR-216a suppressed metastasis of GC. [score:5]
Figure 8 (A) SGC-7901 cells that were transfected with miR-216a inhibitors (anti-miR-216a) were treated with the JAK2 inhibitor SAR317461 and DMSO, respectively. [score:5]
JAK2 mRNA and protein expression levels were determined after miR-216a overexpression. [score:5]
Interestingly, miR-216a overexpression led to increased expression E-cadherin and decreased levels of N-cadherin and Vimentin in MGC-803 cells (P<0.05, respectively, Figure 4A). [score:5]
Thus, we hypothesized that miR-216a inhibited EMT process and metastasis of GC cells probably by targeting JAK2/STAT3 pathway. [score:5]
Potential targets of miR-216a were predicted using the public database TargetScan (http://www. [score:5]
In turn, miR-216a knockdown facilitated EMT process of SGC-7901 cells with decreased E-cadherin and increased N-cadherin and Vimentin expression, as determined by immunoblotting and IF results (P<0.05, respectively, Figure 4C and 4D). [score:4]
miR-216a directly targets JAK2 in GC cells. [score:4]
The JAK2 inhibitor SAR317461 reverses the effects of miR-216a knockdown in GC cells. [score:4]
JAK2 is a direct target of miR-216a in GC cells. [score:4]
Furthermore, the JAK2 inhibitor SAR317461 was used for inactivation of JAK2/STAT3 pathway in miR-216a down -regulating GC cells. [score:4]
SAR317461 treatment blocked JAK2/STAT3 pathway and suppressed migration, invasion and EMT process of SGC-7901 cells with miR-216a knockdown (P<0.05, respectively, Figure 8A-8C). [score:4]
On the other hand, miR-216a was knocked down by miR-216a inhibitors in SGC-7901 cells (P<0.05, Figure 2D). [score:4]
Based on these findings, we suggest that JAK2 is a potential direct target of miR-216a in GC cells. [score:4]
miR-216a was found to be downregulated in GC tissues than in matched non-tumor tissues (P<0.05, Figure 1A). [score:4]
miR-216a underexpression associates with malignant clinical features and poor prognosis of GC patients. [score:3]
The mechanisms underlying the aberrant expression of miR-216a in human cancer is largely unknown. [score:3]
JAK2/STAT3 functions in miR-216a inhibited EMT process and metastasis of GC cells. [score:3]
miR-216a has recently been reported to play a tumor suppressive role in human cancer including glioma [10], colorectal cancer (CRC)[11] and pancreatic cancer [12, 13]. [score:3]
IF results further confirmed the changes of E-cadherin and Vimentin expression after miR-216a restoration (Figure 4B). [score:3]
Figure 2 (A) MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were subjected to qRT-PCR for miR-216a expression. [score:3]
miR-216a inhibits activation of JAK2/STAT3 pathway. [score:3]
Overexpression of miR-216a facilitates EMT and subsequently promotes metastatic behaviors of HCC and ovarian cancer cells [14, 15]. [score:3]
We found that JAK2 restoration promoted the phosphorylation of STAT3 and EMT process, and subsequently facilitated migration and invasion of miR-216a overexpressing MGC-803 cells (P<0.05, respectively, Figure 7A-7C). [score:3]
Functionally, we demonstrated that miR-216a suppressed migration, invasion and EMT process of GC cells in vitro and in vivo. [score:3]
Multivariate Cox regression analysis indicated that miR-216a expression was an independent risk factor for poor prognosis of GC patients (P=0.018, Table 2). [score:3]
The clinicopathological significance of miR-216a expression in GC patients was shown in Table 1. Low level of miR-216a notably correlated with lymph node metastasis, venous infiltration, invasive depth and advanced TNM stage (P<0.05, respectively). [score:3]
miR-216a suppresses EMT process of GC cells. [score:3]
On the other hand, SGC-7901 cells that were transfected with miR-216a inhibitors (anti-miR-216a) or scrambled controls (anti-control) were subjected to immunoblotting. [score:3]
HE staining revealed that miR-216a overexpression significantly reduced the number of metastatic nodes of MGC-803 cells in nude mice livers. [score:3]
miR-216a inhibits migration and invasion of GC cells. [score:3]
miR-216a suppresses liver metastasis of GC cells in mice. [score:3]
Thus, miR-216a underexpression potentially functions as a predictor for poor prognosis of GC patients. [score:3]
Association between the clinicopathological features and miR-216a expression in gastric cancer patients. [score:3]
We disclosed that the expression of miR-216a was restrained in GC. [score:3]
Figure 4 (A) MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were subjected to immunoblotting for E-cadherin, N-cadherin and Vimentin expression. [score:3]
Clinical analysis revealed that miR-216a expression was an independent prognostic factor for predicting poor clinical outcome of GC patients. [score:3]
Previous data demonstrate that miR-216a is involved in tumor initiation and progression, and its underexpression contributes to poor clinical outcome and cellular malignant phenotypes of CRC, pancreatic cancer, glioma and oral squamous cell carcinoma [10- 13, 17]. [score:3]
In this study, JAK2 was identified as a direct target gene of miR-216a in GC cells by a luciferase reporter assay, which was consistent with the results in pancreatic cancer [13]. [score:3]
In conclusion, we demonstrate that the expression of miR-216a is restrained in GC tissues and cell lines. [score:3]
These findings suggest that miR-216a potentially plays an anti-metastatic role GC by targeting JAK2/STAT3 pathway. [score:3]
Furthermore, miR-216a prohibits invasion and migration of CRC cells in vitro, and restrains liver metastasis in vivo by targeting KIAA1199 [11]. [score:3]
The expression and prognostic value of miR-216a in GC. [score:3]
Figure 1 (A) The relative expressions of miR-216a in 90 pairs of GC tissues and matched noncancerous tissues. [score:3]
Moreover, we disclosed that the expressions of miR-216a were reduced in GC cell lines. [score:3]
miR-216a/217 overexpression induces EMT of hepatocellular carcinoma (HCC) cells and promotes recurrence and sorafenib resistance of HCC [15]. [score:3]
Furthermore, low expression of miR-216a correlated with poor prognostic features and conferred a reduced survival in GC patients. [score:3]
Thus, miR-216a exerts its anti-metastatic role probably by targeting JAK2/STAT3 pathway in GC cells. [score:3]
miR-216a overexpression was confirmed by the qRT-PCR results (P<0.05, Figure 2A). [score:3]
To date, the exact role of miR-216a in GC and its target genes are poorly elucidated. [score:3]
miR-216a overexpression led to reduced levels of JAK2, phophorylated STAT3, Slug, Snail and Twist in MGC-803 cells. [score:3]
Precursor miR-216a clones, miR-216a inhibitors and scrambled controls clones were purchased from Genecopoeia (Guangzhou, China). [score:3]
The expression of miR-216a was detected by qRT-PCR in GC and matched noncancerous tissues. [score:3]
The “low” versus “high” miR-216a expression was defined according to the cut-off values of miR-216a level which were defined as the median of the cohort of tested patients. [score:3]
In accordance, miR-216a knockdown promoted activation of JAK2/STAT3 pathway in SGC-7901 cells (P<0.05, respectively, Figure 6). [score:2]
miR-216a knockdown promoted migration and invasion of SGC-7901 cells (P<0.05, respectively, Figure 2E and 2F). [score:2]
These results indicate that miR-216a inversely regulates EMT process of GC cells. [score:2]
miR-216a knockdown promoted activation of JAK2/STAT3 pathway in SGC-7901 cells. [score:2]
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]
Subsequent study demonstrated that miR-216a expression was strongly reduced in GC cells (SGC-7901, MGC-803, MKN-28, and BGC-823 compared to GES-1 cells (P<0.05, respectively, Figure 1B). [score:2]
These data suggest that miR-216a exhibits an anti-metastatic role in the development of GC. [score:2]
Therefore, it is valuable to study the regulatory effects of miR-216a in EMT process and metastasis of GC cells. [score:2]
miR-216a retrains EMT process of GC cells. [score:1]
Next, we disclosed whether JAK2 mediated the role of miR-216a in migration, invasion and EMT process of GC cells. [score:1]
miR-216a restrains pancreatic tumor growth via inducing G2/M arrest and apoptosis by decreasing lncRNA MALAT1 [12]. [score:1]
MGC-803 cells that were transfected with precursor miR-216a or scrambled controls were injected through the tail vein of nude mice and cultivated for 9 weeks. [score:1]
In contrast, no changes in relative luciferase activity were observed when the miR-216a binding site was mutated. [score:1]
Thus, the underlying mechanisms responsible for miR-216a underexpression require further investigation. [score:1]
In this study, we were aimed to investigate the expression and biological function of miR-216a in GC. [score:1]
Next, to determine the role of miR-216a in GC cells, we transfected MGC-803 cells with precursor miR-216a and scrambled controls (miR-control), respectively. [score:1]
Altogether, our data indicate that miR-216a plays an anti-metastatic role in GC cells. [score:1]
In contrast, no changes in relative luciferase activity were observed when the miR-216a binding site was mutated (Figure 5D). [score:1]
org), and the putative complementary sequence of miR-216a was identified in the 3′-UTR of JAK2 mRNA, as illustrated in Figure 5A. [score:1]
In addition, liver metastasis mo del showed that miR-216a overexpresion significantly reduced the number of metastatic nodules in livers arising from nude mice (P<0.05, Figure 3). [score:1]
Representative IHC data showed that strong staining of JAK2 was observed in GC tissues with low miR-216a level, while weak signal of JAK2 was detected in cases with high miR-216a level (Figure 5F). [score:1]
On the contrary, miR-216a facilitates epithelial-mesenchymal transition (EMT) of ovarian cancer cells and subsequently promotes migration and invasion of tumor cells [14]. [score:1]
The JAK2 levels in high-miR-216a PADCs were significantly lower than that of those low-miR-216a GCs. [score:1]
Figure 5 (A) The potential miR-216a binding site in wild type (wt) 3’-UTR sequence of JAK2. [score:1]
Figure 6MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were detected by immunoblotting. [score:1]
As shown in Figure 5D, cells transfected with wt JAK2 3′-UTR vector containing a precursor miR-216a showed significantly lower luciferase activity than cells transfected with miR-control (P<0.05). [score:1]
, (Guangzhou, China) Small nuclear RNA U6 and GAPDH mRNA were used as internal controls for calculating the relative expression levels of miR-216a and JAK2 via the 2 [-ΔΔCt] method. [score:1]
MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were intravenously injected into tail vein in nude mice. [score:1]
Subsequently, Spearman correlation analysis revealed that JAK2 mRNA levels were negatively correlated with miR-216a levels in GC tissues (r=-0.529, P=0.006, Figure 5E). [score:1]
Accordingly, we demonstrated that JAK2 restoration abrogated the anti-metastatic effects of miR-216a on GC cells with enhanced migration, invasion and EMT progression. [score:1]
MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were detected by immunoblotting. [score:1]
These studies suggest that the role of miR-216a is a controversial topic in different cancers. [score:1]
In addition, GC patients with low miR-216a level showed a significant shorter survival (P<0.05, Figure 1C). [score:1]
Figure 3MGC-803 cells that were transfected with precursor miR-216a (pre-miR-216a) or scrambled controls (miR-control) were intravenously injected into tail vein in nude mice. [score:1]
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2
[+] score: 102
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]
The analysis for the KC animals compared to controls revealed that miR-150, miR-494, miR-138, miR-148a*, miR-216a, and miR-217 (p-value = 0.01) were significantly downregulated (Table 1), whereas, miR-146b, miR-205, miR-31, miR-192, and miR-21 (p-value = 0.01) were significantly upregulated (Table 2). [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: 36
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
In our results, miR-21a, miR-31, miR-200c and miR-155 were upregulated and miR-217, miR-802, miR-375 and miR-216 were downregulated (Additional file 9: Table S5). [score:7]
AC Azevedo-Pouly, DS Sutaria, J Jiang, OA Elgamal, F Amari, D Allard, et al. miR-216 and miR-217 expression is reduced in transgenic mouse mo dels of pancreatic adenocarcinoma, knockout of miR-216/miR-217 host gene is embryonic lethal. [score:4]
In downregulated miRNAs, miR-216a-3p/5p, miR-216b-3p/5p, miR-217-5p, miR-802-3p/5p and miR-375-3p lay on the top. [score:4]
miR-216/miR-217 were supposed to be reduced in pancreatic adenocarcinoma [37]. [score:1]
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4
[+] score: 25
In experimental diabetic nephropathy mo dels, TGF-β and miR-192 upregulate miR-216 and 217, which in turn inhibit their target molecule, Pten, resulting in Akt activation, survival and hypertrophy of glomerular mesangial cells [14]. [score:8]
In addition, the frequencies of apoptosis -associated target genes of miR-192, miR-216a, and miR-217, all previously reported to be regulated by TGF-β in kidney disease [12- 14, 31], were not significantly different from random control miRNAs (Figure 2C). [score:6]
For example, extensive work has demonstrated that the upregulation of miR-192 [12] and miR-216a/miR-217 [14] by TGF-β in mesenchymal glomerular mesangial cells can switch off E-Box transcriptional repressors, resulting in increased collagen synthesis [12], and turn on Akt by repressing its inhibitor, PTEN, promoting mesangial cell survival and hypertrophy [14]. [score:6]
C. Bar graph shows the fraction of genes annotated with the biological process, ‘apoptosis’ (Ingenuity Systems), among all the predicted target genes of TGF-β-regulated miR-30s, miR-192, miR-216a, and miR-217 or the mean ± S. D. of 20 randomly chosen miRs that are not known to be regulated by TGF-β (control). [score:5]
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5
[+] score: 13
Interestingly, another miRNA, miR-216a, that is also downstream of TGF-β signaling and miR-192, has been shown to target BECN1 and ATG5 expression in endothelial cells and Becn1 in pancreatic cancer cells 40, 53, 54. miR-216a also plays a pathogenic role in DN by up -regulating collagen genes through TFE3 by targeting YBX-1 [55]. [score:8]
Overall, it is likely that the inhibitory effect of miR-192 on autophagy genes is mediated by these miRNAs (miR-216a, 217 and 200) which are induced by miR-192 (Fig.   7) 39, 40. [score:3]
We have previously shown that miR-192 can mediate fibrotic effects of TGF-ß and plays a key role in the pathogenesis of DN in MC 37, 38. miR-192 is also part of a cascade of downstream miRNAs (including miR-200, miR-216a, miR-217) that also regulate fibrotic genes and contribute to the pathogenesis of DN 39, 40. [score:2]
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6
[+] score: 13
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-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-216b, 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]
MicroRNA-216a/217 -induced epithelial-mesenchymal transition targets PTEN and SMAD7 to promote drug resistance and recurrence of liver cancer. [score:2]
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7
[+] score: 12
Amylase and lipase increases were noted from 1–8 h in rats in both 15 and 50 μg/kg dose groups while pancreatic necrosis was noted at 8, 24 and 48 h. MiR-375-3p has been reported to be enriched in islets and the miRNA with the highest intra-islet expression [38] and in our study was increased from 4–24 h in the 15 and 50 μg/kg groups, returning to approximately vehicle level by 48 h. MiR-216a-5p and miR-217-5p remained elevated in the serum of rats longer than amylase or lipase and had a much greater dynamic range which could be advantageous if detection of pancreatic injury is not able to be examined at earlier time points. [score:3]
Based on these studies miR-216a-5p displayed the largest dynamic range and correlated well with amylase and lipase indicating that it is the best translatable miRNA biomarker that correlated to pancreatic injury from rat to dog. [score:3]
MiR-216a-5p, amylase and lipase were increased in the serum concurrently at 1 h, remained elevated until 8 h while miR-216a-5p remained elevated until 24 h. MiR-217-5p displayed similar kinetics to miR-216a-5p except miR-217-5p generally had a larger dynamic range and remained elevated until 48 h. Both miRs-216a-5p and 217-5p displayed much larger dynamic ranges than amylase or lipase and remained elevated longer. [score:1]
Finally, we determined that miR-216a-5p appears to perform as well or better as a marker of pancreatic injury than amylase, lipase or other pancreas enriched miRNAs in rat and dog caerulein toxicity studies. [score:1]
It is possible that additional pancreas specific and/or enriched miRNAs may supplement the interpretation of pancreatic injury or serve as better biomarkers than miR-216a-5p in pancreatic toxicity studies utilizing different pancreatic toxicants. [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]
MiR-141-3p and miR-216a-5p were increased beyond vehicle treated dogs and did not display consistent time dependent increases. [score:1]
miRNAs were dose dependently increased in the serum of dogs treated with 15 and 45 ug/kg of caerulein and correlated to amylase and lipase increases while miR-216a-5p remained elevated until 24 h. Values are normalized to vehicle and to the cel-miR-55-3p spike in Conserved pancreas tissue enriched miRNAs were examined in the rat and dog mo dels of caerulein pancreatic toxicity in order to begin to characterize miRNAs as species translatable serum based biomarkers of pancreatic injury (Table  2). [score:1]
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[+] score: 8
Recently, miRNA expression profiles [19] revealed that several miRNAs (miR-192, miR-194, miR-204, miR-215, and miR-216) are highly and nearly exclusively expressed in the kidney. [score:5]
TGF-β1 positively regulates miR-192 [20] and miR-216a [22] but negatively regulates the miR-200 family [52], resulting in enhanced ECM protein accumulation, which contributes to DN pathogenesis. [score:3]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-216a, hsa-mir-217, mmu-mir-217, gga-mir-216a, gga-mir-217
KRAS is upregulated in different cancer types, and post-transcriptional regulation of KRAS via interaction with miR-216a/217 was reported in vitro (36). [score:5]
These (and even shorter) isoforms also are no longer responsive to the validated regulation of KRAS by miR-216a/217. [score:2]
The other variants with shorter 3′UTRs, however, loose between 16 and 36 potential miRNA binding sites, and among these are the experimentally validated binding sites of miR-216a and miR-217. [score:1]
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10
[+] score: 7
Other miRNAs from this paper: mmu-mir-126a, mmu-mir-216b, mmu-mir-216c, mmu-mir-126b
We previous reported that CCN1 promotes VEGF-A expression in osteoblasts and subsequently enhances angiogenesis through the inhibition of miR-216 during RA disease [20]. [score:7]
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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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[+] score: 6
Further, miR-216a and miR-217, both of which target PTEN, activate Akt through PTEN down-regulation in kidney disorders [61]. [score:6]
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[+] score: 5
Recent studies have suggested important regulatory roles for miRNAs such as miR-21, miR-216, miR-217, miR-181b, miR-31b and miR-34a, which were confirmed to be upregulated in senescing HUVECs (Menghini et al., 2009), and miR-146, miR-142-3p, miR-223 and miR-29 family members, which were significantly increased in whole aortas of aged mice (Zhao et al., 2010). [score:5]
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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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In the past few years, a number of studies of miRNAs in AD have emerged to support that deregulated miRNAs, such as miR-18b, miR-34c, miR-615, miR-211, miR-216 and miR-325, play important roles in the development and prognosis of AD [16]. [score:3]
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[+] score: 3
Among the known ~2,500 miRNA by deep sequencing of human genome [12], miR-192, miR-194, miR-204, miR-215 and miR-216 are highly expressed in kidney than other human tissues [13]. [score:3]
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Li H MiR-216a rescues dexamethasone suppression of osteogenesis, promotes osteoblast differentiation and enhances bone formation, by regulating c-cbl -mediated PI3K-AKT pathwayCell Death Differ. [score:3]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-216a
Gong D. Cheng H. P. Xie W. Zhang M. Liu D. Lan G. Huang C. Zhao Z. W. Chen L. Y. Yao F. Cystathionine γ-lyase (CSE)/hydrogen sulfide system is regulated by miR-216a and influences cholesterol efflux in macrophages via the PI3K/AKT/ABCA1 pathway Biochem. [score:2]
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[+] 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-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, hsa-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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[+] 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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These are mir-17, mir-22, mir-28, mir-32, mir-128b, mir-135b, mir-143, mir-151, mir-181b-2, mir-205, mir-213, mir-216 and mir-372. [score:1]
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816 miR-216a −1.093 −41.184 1 was performed with a pool of miRNAs from frozen gastric biopsies from 4 infected and 3 NI d3Tx mice. [score:1]
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[+] score: 1
However, ISH detection of other retina-specific miRs, including miR-213, miR-216, and miR-217, was unsuccessful in retina [26, 27]. [score:1]
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To date only few lncRNAs have been reported as hosts for some miRNAs under diabetic conditions, for e. g., RP23-298H6.1-001 hosting miR-216a and miR-217 (refs 6, 11, 28, 29, 30). [score:1]
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