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11 publications mentioning hsa-mir-1291

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1291. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 346
Our study using two-dimensional difference gel electrophoresis (2D-DIGE), matrix-assisted laser desorption/ionization (MALDI)-time of flight (TOF) and MS/MS analyses revealed 19 downregulated proteins and 13 upregulated proteins whose levels were altered over 2-fold in miR-1291 -expressing PANC-1 cells (Table 1, Figure 5A–5C). [score:9]
Although many genes encoding those altered proteins in miR-1291 -expressing PANC-1 cells do not seem to be directly regulated by miR-1291, the present study identified FOXA2 as a direct target for miR-1291. [score:8]
We first showed that miR-1291 was significantly downregulated in patient PDAC tissues, and restoration of miR-1291 expression/function inhibited pancreatic cancer cell proliferation in vitro through induction of G2/M cell cycle arrest and enhancement of apoptosis. [score:8]
In addition, the extent of decrease in AGR2 protein levels was greater than that of FOXA2 in miR-1291 -expressing PANC-1 cells, suggesting the presence of other pathways and an accumulative effect on the suppression of AGR2 expression. [score:7]
While bioinformatics analyses indicated that AGR2 did not appear to be a direct target of miR-1291, FOXA2, the transcription regulator of AGR2 [35– 37], was predicted to be a potential target of miR-1291. [score:7]
Indeed the lower level of AGR2 protein expression in miR-1291 -expressing PANC-1 (Figure 8A) and AsPC-1 (Figure 8B) cells was associated with a reduced level of FOXA2 protein expression. [score:7]
Oncogenic AGR2 was identified as the most significantly downregulated protein in miR-1291 -expressing PANC-1 cells with lower capacity in proliferation and tumorigenesis, consistent with previous findings on the critical role of AGR2 in pancreatic cancer [38, 40]. [score:6]
The overexpression of AGR2 (Figure 7) and downregulation of miR-1291 (Figure 1B) in pancreatic carcinoma indicates an inverse relationship between miR-1291 and AGR2 in pancreatic cancer. [score:6]
Other studies showed that miR-1291 is downregulated in clinical renal cell carcinoma specimens [33], and gain of miR-1291 function inhibits the proliferation, migration and invasion of renal carcinoma A498 and 786-O cells [34]. [score:6]
miR-1291 modulates AGR2 expression through targeting of FOXA2, a known transcriptional regulator of AGR2. [score:6]
It is possible that other genes and pathways might be also involved in miR-1291-caused downregulation of AGR2 (as well as changes of other proteins listed in Table 1) in suppressing the proliferation and tumorigenesis of pancreatic cancer cells. [score:6]
The protein downregulated in miR-1291 -expressing PANC-1 cells to the greatest degree was identified as AGR2. [score:6]
Our results demonstrated that miR-1291 was significantly downregulated in pancreatic cancer specimens, which was in contrast to the overexpression of oncogenic AGR2. [score:6]
These results, along with the previous findings on the regulation of AGR2 by FOXA2 [35– 37], demonstrate that miR-1291 modulates AGR2 expression via targeting of its transcription factor FOXA2. [score:6]
Figure 7AGR2 is overexpressed in patient PDAC tissues, which is in contrast to the reduced expression of miR-1291 (Figure 1B)(A, B) AGR2 mRNA levels were significantly higher in pancreatic tumor tissues than non-tumor tissues, as determined by selective qPCR analyses. [score:5]
Consistent with our recent findings on the antiproliferative activity of miR-1291 [31], this study further demonstrated that restoration of miR-1291 expression/function significantly inhibited the growth of human pancreatic cancer cells, which was associated with an accumulation of cells in G2/M phase and larger fractions of apoptotic cells. [score:5]
Difference in global protein expression profiles between miR-1291 -expressing and control PANC-1 cells. [score:5]
To understand possible signaling pathways underlying miR-1291-controlled suppression of pancreatic tumorigenesis, an unbiased comprehensive proteomic profiling study was conducted to determine global protein expression altered by miR-1291 (Figure 5). [score:5]
Proteins differentially expressed in miR-1291 -expressing and control PANC-1 cells, which were identified by 2D-DIGE, MALDI-TOF and MS/MS proteomic profiling study. [score:5]
Our data also demonstrated that re-introduction of miR-1291 to pancreatic cancer cells remarkably suppressed tumorigenesis in xenograft mouse mo dels, which might be attributable to the inhibition of cell proliferation, induction of G2/M cell cycle arrest, and enhancement of apoptosis. [score:5]
Furthermore, consistent with the results obtained from miR-1291 -expressing pancreatic cancer cells (this study), both FOXA2 and AGR2 protein levels were reduced in cells after transient transfection with miR-1291 expression plasmids (data not shown) or bioengineered miR-1291 agent [31]. [score:5]
In addition, miR-1291 was revealed to largely suppress the tumorigenesis of PANC-1 cells, in which the same mouse was inoculated with both miR-1291 -expressing and control PANC-1 cells. [score:5]
In addition, the transcription regulator of AGR2, forkhead box protein A2 (FOXA2) [35– 37], was identified as a direct target of miR-1291. [score:5]
Our efforts were thus directed to understand how miR-1291 might regulate AGR2 expression in pancreatic cancer cells. [score:5]
Consequent luciferase reporter assays showed that gain and loss of miR-1291 expression/function was able to significantly reduce and increase FOXA2 3′UTR luciferase activities, respectively (Figure 8D and 8E), supporting that FOXA2 is a direct target of miR-1291. [score:5]
AGR2 is overexpressed in patient PDAC tissues, which is in contrast to the reduced expression of miR-1291 (Figure 1B). [score:5]
Restoration of miR-1291 expression suppresses the proliferation of PANC-1 and AsPC-1 cells. [score:5]
In addition, FOXA2 was revealed as a direct target for miR-1291, which connected miR-1291 to the established FOXA2-AGR2 regulatory pathway [35– 37] in the control of pancreatic cancer cell properties. [score:5]
MiR-1291 expression is downregulated in human pancreatic cancer cell lines and patient tumor specimens. [score:5]
Furthermore, restoration of miR-1291 expression inhibited pancreatic cancer cell proliferation that was attributed to the induction of G2/M cell cycle arrest and apoptosis. [score:5]
Actually AGR2 protein levels were reduced to different degrees in miR-1291 -expressing PANC-1 and AsPC-1 cells, highlighting intrinsic difference in the regulatory pathways beyond miR-1291-FOXA2-AGR2 between the two cells lines. [score:4]
The present study is the first to find that miR-1291 is significantly downregulated in patient pancreatic carcinoma tissues and pancreatic cancer cell lines. [score:4]
While further biological experiments are necessary to validate FOXA2 as a direct target of miR-1291, this study has firmly established the impact of miR-1291 on FOXA2. [score:4]
Because AGR2 was down-regulated to the greatest extent in miR-1291 -expressing PANC-1 cells and AGR2 is a known proto-oncogene in the control of cancer cell proliferation, invasion and transformation [38– 41], the clinical PDAC samples (Figure 1B) were thus employed to critically evaluate the relationship between miR-1291 and AGR2. [score:4]
Therefore, further studies on additional targets of miR-1291 are necessary to provide an improved mechanistic understanding of miR-1291 pathways in the regulation of pancreatic cancer processes. [score:4]
Together, our results link miR-1291 to FOXA2-AGR2 regulatory pathway in the suppression of pancreatic tumorigenesis. [score:4]
These findings improve the understanding of pancreatic miRNA oncotargets and provide insight that supports the development of miR-1291 -based therapy for the treatment of pancreatic cancer. [score:4]
Then we demonstrated miR-1291 sharply suppressed tumorigenicity of PANC-1 cells in xenograft mouse mo dels in vivo. [score:3]
miR-1291 suppresses the tumorigenicity of PANC-1 cells in xenograft tumor mouse mo dels. [score:3]
The decreased expression of miR-1291 found in human pancreatic cancer cell lines and PDAC tissues suggest that miR-1291 might be related to pancreatic tumorigenesis. [score:3]
Our recent studies have identified that microRNA-1291 (miR-1291), a less studied miRNA that is generated from small nucleolar RNA H/ACA box 34 (SNORA34) in pancreatic cancer PANC-1 cells, is able to increase intracellular drug accumulation and chemosensitivity through targeting of efflux transporter namely multidrug resistance -associated protein 1 (MRP1/ABCC1) [30, 31]. [score:3]
Figure 4(A) Representative picture of mouse inoculated with control and miR-1291 -expressing PANC-1 cells. [score:3]
The data revealed that growth of PANC-1 xenograft tumors in the same mouse was remarkably and significantly suppressed by miR-1291 (Figure 4A and 4B). [score:3]
Several targets identified for miR-1291 thus far include the efflux transporter ABCC1 underlying multidrug resistance [30], the endoplasmic reticulum stress sensor IRE1α and consequently glypican-3 (GPC3) implied in liver carcinogenesis [43, 44], glucose transporter protein type 1 (GLUT1/SLC2A1) critical for cell metabolism [34], and mucin 1 (MUC1) making up mucus [42]. [score:3]
Proteins were extracted from miR-1291 -expressing PANC-1 cells and control cells, and subjected to 2D-DIGE and protein identification by MALDI-TOF and tandem MS (Applied Biomics, Hayward, CA), as described [57, 58]. [score:3]
Besides FOXA2, several other cancer-related genes such as protein kinase B AKT2 [50– 52] and methyl-CpG binding protein 2 (MeCP2) [53– 55] were also identified as putative targets for miR-1291 by computational analysis. [score:3]
These results indicate that miR-1291 is able to suppress the tumorigenicity of pancreatic cancer cells in xenograft mouse mo dels. [score:3]
Nevertheless, consistent results are obtained from present and previous studies [31, 32, 34, 42], indicating that miR-1291 acts as a tumor suppressor in renal, esophageal squamous, and pancreatic cancer cells. [score:3]
We thus generated stable miR-1291 -expressing AsPC-1 and PANC-1 cells to explore potential mechanisms. [score:3]
To further define the impact of miR-1291 on the tumorigenesis of pancreatic cancer cells, miR-1291 -expressing and control PANC-1 cells were injected subcutaneously into the right and left side of the dorsum of nude mouse, respectively, and outgrowth of xenograft tumors was monitored. [score:3]
Figure 3(A, B) Comparison of flow cytometry histograms of control and miR-1291 -expressing PANC-1 cells stained with propidium iodide, and (C) the percentage of cells at various phases (G1/G0, S and G2/M). [score:3]
miR-1291 expression levels are lower in human pancreatic cancer cell lines and patient PDAC tissues. [score:3]
We then examined miR-1291 expression levels in patient PDAC tissues in comparison to normal pancreatic tissues. [score:3]
The miR-1291 expression plasmid and the control empty vector were described recently [30]. [score:3]
The protein levels of AKT2 and MeCP2 were indeed reduced in miR-129 -expressing PANC-1 cells (unpublished data) or MCF-7 cells transiently transfected with miR-1291 agent [31]. [score:3]
Exponentially growing control and miR-1291 -expressing PANC-1 cells were harvested, resuspended in 100 μL of PBS/Matrigel (1:1) solution and injected subcutaneously (10 million cells/animal) into nude mice (12 per group). [score:3]
Figure 1(A) The expression levels of miR-1291 were remarkably lower in human pancreatic cancer cell lines than other cell lines. [score:3]
In conclusion, the present study revealed a miR-1291-FOXA2-AGR2 signaling pathway behind miR-1291-controlled suppression of pancreatic tumorigenesis. [score:3]
Together, these results demonstrate that miR-1291 inhibits pancreatic cancer cell proliferation (Figure 2) via the induction of G2/M cell cycle arrest and enhancement of early apoptosis (Figure 3). [score:3]
HepG2 cells were co -transfected with FOXA2 3′UTR luciferase expression plasmid and 50 nM miR-1291 antagomir or control oligonucleotides. [score:3]
A sharp reduction of AGR2 (current study) and significant change of cell metabolome [32] are unified for miR-1291 -expression PANC-1 cells, suggesting that miR-1291 may be implicated in the metabolism of pancreatic cancer cells. [score:3]
The coding sequence of FOXA2 (NM_021784.4) 3′UTR segment (0–830 bp from stop codon) consisting of miR-1291 MRE sites that were predicted by TargetScan (http://www. [score:3]
In addition, xenograft tumors derived from miR-1291 -expressing PANC-1 cells were much smaller (Figure 4C) and over 10-fold lighter (Figure 4D) than the paired specimens generated from control PANC-1 cells. [score:3]
Figure 5(A–C) 2D-DIGE images of proteins in the control and miR-1291 -expression PANC-1 cells labeled with green and red fluorescent dye, respectively, and the overlaid graph indicating the difference in the abundance of proteins. [score:3]
The miR-1291 -expressing and control PANC-1 cells were established recently in our lab [30]. [score:3]
These findings improve our understanding of pancreatic cancer and critical regulatory pathways which provide insight into the development of miR-1291 -based therapeutic strategy. [score:3]
In addition, the fraction of early apoptotic cells was increased by 40% in miR-1291 -expressing PANC-1 cells (Figure 3D–3F). [score:3]
Restoration of miR-1291 expression reduces human pancreatic cancer cell proliferation by inducing G2/M cell cycle arrest and enhancing apoptosis. [score:3]
AsPC-1 cells stably transfected with miR-1291 expression plasmid and empty control vector were developed in the same manner. [score:3]
Recent studies have showed that miR-1291 level is lower in renal cell carcinoma specimens [33] and esophageal squamous cell carcinoma [42], and restoration of miR-1291 suppresses renal and esophageal squamous cancer cell proliferation, migration and invasion [34, 42]. [score:3]
Briefly, PANC-1 cells were co -transfected with FOXA2 3′UTR luciferase reporter plasmid and miR-1291 expression or control plasmid. [score:3]
MiR-1291 modulates the expression of many proteins in PANC-1 cells that are assembled into a network of tumor regulatory pathways. [score:3]
Our data showed that restoration of miR-1291 expression led to a 2-fold increase of PANC-1 cells in G2/M phase, which was accompanied by a significant reduction of cells in G1 phase and increase of cells in S phase (Figure 3A–3C). [score:3]
Most importantly, this study found that a series of cell metabolism-related proteins such as ASS1, OAT, UGDH, and PCK2 were significantly altered in miR-1291 expressing cells. [score:3]
Figure 2(A, B) miR-1291 expression levels were about 9- and 12-fold higher in miR-1291 stably transfected PANC-1 and AsPc-1 cells, respectively, as compared to corresponding control cells transfected with empty vectors. [score:2]
AsPC-1 and PANC-1 cells transiently transfected with miR-1291 expression plasmid exhibited about 50% lower viabilities, compared to cells transfected with empty vectors (data not shown). [score:2]
Compared to corresponding controls, miR-1291 -expressing PANC-1 and AsPC-1 cells showed approximately 9- (Figure 2A) and 12-fold (Figure 2B) higher miR-1291 levels, which resulted in a significantly lower cell proliferation capacity (Figure 2C and 2D). [score:2]
These results suggest that miR-1291 modulates a network of important tumor-regulatory pathways in pancreatic cancer cells. [score:2]
Furthermore, we identified a set of proteins altered in PANC-1 cells by miR-1291 that were assembled into critical tumor regulatory pathways. [score:2]
Figure 8(A, B) analysis showed that both FOXA2 and AGR2 protein levels were much lower in miR-1291 -expressing PANC-1 (A) and AsPC-1 (B) cells, as compared to corresponding control cells. [score:2]
MiR-1291 suppresses the tumorigenicity of human pancreatic cancer cells in mouse mo dels. [score:2]
Therefore, current study unveiled the connection between miR-1291 and FOXA2-AGR2, namely miR-1291-FOXA2-AGR2 pathway, in the modulation of pancreatic cancer cellular processes. [score:1]
Proteomic profiling study revealed a set of proteins altered by miR-1291 that formed a network of interactions in the control of critical cancer properties. [score:1]
To delineate the potential role of miR-1291 in pancreatic cancer, we first investigate the effects of restoration of miR-1291 expression/function on pancreatic cancer cell proliferation. [score:1]
A more striking difference was seen in the five sets of paired specimens in which miR-1291 levels were 6-fold lower in tumor samples than their paired normal pancreatic tissues (Figure 1B). [score:1]
Underlined is the seed sequence of miR-1291. [score:1]
We have also demonstrated that miR-1291 modulates the metabolome of PANC-1 cells and reduces cell migration and invasion capacity [32]. [score:1]
Our recent metabolomics study have revealed nicotinamide N-methyltransferase (NNMT), an enzyme participating in nicotinate and nicotinamide metabolism, as a biomarker for miR-1291-altered pancreatic cancer cell metabolome [32]. [score:1]
MiR-1291 belongs to a special group of miRNAs that are derived from small nucleolar RNAs [30]. [score:1]
Proteins identified above that were altered in PANC-1 cells by miR-1291 were mapped into molecular networks using Ingenuity Pathway Analysis (IPA) (www. [score:1]
The network of interactions among miR-1291-modualted proteins. [score:1]
To assess whether the inhibition of pancreatic cancer cell proliferation by miR-1291 involves mechanistic changes of cell cycle and apoptosis, we measured cell cycle (Figure 3A–3C) and apoptotic (Figure 3D–3F) profiles through flow cytometric analyses of propidium iodide and Annexin V/propidium iodide stained cells, respectively. [score:1]
As shown in Figure 1B, miR-1291 levels were about 60% lower in PDAC tissues than unpaired non-tumor tissues. [score:1]
Regular and stem-loop reverse transcription of mature miR-1291 were conducted as described previously [30, 60]. [score:1]
Since PANC-1 cells were more sensitive to miR-1291 than AsPC-1 cells, PANC-1 cell lines were utilized for further studies. [score:1]
Reintroduction of miR-1291 into PANC-1 cells induces a G2/M cell cycle arrest and an enhanced apoptosis. [score:1]
The current study revealed a significantly lower miR-1291 level in pancreatic tumor specimens as well as pancreatic cancer cell lines. [score:1]
The objective of the current study was to delineate the role of miR-1291 in pancreatic cancer. [score:1]
The input was all miR-1291-altered proteins (in bold) in PANC-1 cells identified by 2D-DIGE, MALDI-TOF and MS/MS proteomic profiling study. [score:1]
In addition, pathway analysis demonstrated that miR-1291-altered proteins formed a network of interactions in the modulation of many cancer cellular processes including cell proliferation, cell cycle arrest, invasion, endoplasmic reticulum stress, and energy metabolism (Figure 6). [score:1]
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[+] score: 22
However, when we analysed the predicted targets and GO process, we found that miR-1291 (miRNA with unknown role in the testis) had as target DNA methyltransferases (Dnmt3a, Dnmt3b) (Table  3) involved in de novo histone methylation, genomic imprinting, X-chromosome inactivation and testicular germ cell tumours due to exposure to alkylphenols 57, 58. [score:5]
Luo H miR-1291 targets mucin 1 inhibiting cell proliferation and invasion to promote cell apoptosis in esophageal squamous cell carcinomaOncol. [score:5]
In conclusion, chronic exposure to a mixture of five EDCs induces changes in the expression profiles of specific miRNAs (such as miR-34b-5p, miR-7686-5p and miR-1291), along with alterations in the miRNAs/isomiRs association (in particular for miR-15b-5p, miR-18b-5p, miR-20b-5p, and miR-1981-5p) regulating mRNAs implicated in key biological process in the testes (Table  3). [score:4]
On the other hand, we found eight down-regulated miRNAs, some of them implicated in multiple processes such as cancer (miR20b-5p, miR-1291) 52, 53, organ injury in toxicity drug mo dels (miR-382-5p) [54], metabolic processes and steroidogenesis (miR-378b) [55], and tissue inflammation (miR-3085-3p) [56]. [score:4]
This suggests that the down-regulation of sncRNAs such as miR-1291 due to exposure to an EDCs-mixture might promote changes in the DNA methylation pattern related to the epigenetic transmission of adverse effects [59]. [score:4]
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[+] score: 16
It has been reported that miR-326 and miR-133a reduce adriamycin resistance of human hepatoma HepG2 cells through downregulating ABCC1 expression [18]; miR-1291 could modulate cellular drug disposition through direct targeting ABCC1 in PANC-1 cells [19]. [score:9]
We analyzed breast cancer dataset from TCGA and found that the levels of miR-326, miR-133a and miR-1291 were all very low, previously reported miRNAs targeting MRP1 in other cancers [18, 19] and their expression levels showed no markedly significant difference in tumors compared to their normal adjacent tissues in breast cancer (Supplementary Figure S1). [score:4]
miR-1291 has been demonstrated to affect drug disposition and increase chemosensitivity by targeting MRP1 in PANC-1 cells [19]. [score:3]
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[+] score: 11
In addition to the previously described miR-124a, FOXA2 is also a direct target for miR-1291, a less studied suppressive miRNA which is generated from small nucleolar RNA H/ACA box 34 in pancreatic cancer cells [34, 35]. [score:6]
Based on these results, Tu et al connected miR-1291 to the FOXA2/AGR2 regulatory pathway in the suppression of pancreatic cancer cell proliferation. [score:4]
Meanwhile, miR-1291 modulates a lot of proteins to form a network of interactions in the control of cancer properties. [score:1]
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[+] score: 3
They may have consensus sequences (hsa-mir-1291 and snoRNA_AJ609443) or show large divergences (hsa-mir-1246 and snRNA_X59360). [score:1]
For example, hsa-mir-1291 shared a consensus sequence with snoRNA_AJ609443 (Figure 3A). [score:1]
Seven human miRNAs (hsa-miR-1291, hsa-miR-1246, hsa-miR-1248, hsa-miR-1274b, hsa-miR-1973, hsa-miR-4284 and hsa-miR-3656) could be accurately mapped to other ncRNAs, which included snoRNAs, snRNAs, tRNAs and rRNAs (Table 1). [score:1]
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[+] score: 3
miRNAs selected for validation studies spanned a range of expression from high to single alignments, and included miR-21, miR-30, miR-98/Let7 family members, miR-221, miR-222, miR-622, miR-664, miR-1248 and miR-1291. [score:3]
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[+] score: 2
The miRNA hairpins of miR-664 and miR-1291 have short 3′ and 5′ regions respectively that do not overlap with a snoRNA. [score:1]
In all three cases, between 75% (mir-1291) and 97% (mir-1248) of the miRNA hairpin is contained within the snoRNA (using the coordinates of the UCSC Genome Browser as described in the ). [score:1]
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[+] score: 2
Furthermore, it has been reported that several circulating miRNAs, such as miR-133, miR-1291, miR-663b, miR-328, and miR-134, exhibit clinical impact on human myocardial infarction [47, 48]. [score:1]
Peng L. Chun-guang Q. Bei-fang L. Xue-zhi D. Zi-hao W. Yun-fu L. Yan-ping D. Yang-gui L. Wei-guo L. Tian-yong H. Clinical impact ofcirculating miR-133, miR-1291 and miR-663b in plasma of patients with acute myocardial infarction Diagn. [score:1]
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[+] score: 2
14 out of 20 (70%) miRNAs were reported to be associated with cancers, and four out of them, namely, hsa-mir-1291, hsa-mir-200b, hsa-mir-134, and hsa-mir-218-2 were directly associated with the renal cell carcinoma. [score:2]
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[+] score: 1
Among the Hadza hunter-gatherers, we found two high frequency PSMAs with allele frequency ≥ 50% in the Hadza only, a novel “A/C” SNP in the stem-loop of hsa-mir-1291 and an “A/G” SNP (rs111566161) in the 3’ mature sequence of miRNA hsa-mir-4711. [score:1]
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[+] score: 1
For example, two host genes, KANSL2 and SNORA34, include hsa-miR-1291. [score:1]
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