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miRBase |
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![]() 7 publications mentioning mmu-mir-873aOpen access articles that are associated with the species Mus musculus and mention the gene name mir-873a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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Other miRNAs from this paper: mmu-mir-211, mmu-mir-873b
Inhibition of miR-873 expression resulted in upregulation of CSMD3 in several hepatoma cell lines, indicating that CSMD3 is indeed a target of miR-873.
[score:10]
The results showed that only upregulation of miR-873 and downregulation of its putative target genes, CSMD3 (CUB and Sushi multiple domains 3) and ATP8B2 (ATPase, aminophospholipid transporter, class I, type 8b, member 2), were consistently verified.
[score:9]
To inhibit miR-873 expression in human and murine hepatoma cell lines, miR-873 inhibition plasmid was purchased.
[score:7]
On the other hand, when miR-873 was overexpressed, suppression of CSMD3 expression was observed in Mahlavu, BNL and Hep-Y2 cells.
[score:7]
Interestingly, following miR-873 upregulation, GRP78 expression was enhanced in most of the hepatoma cell lines.
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After verification process, only miR-873 -mediated downregulation of CSMD3 expression was consistently confirmed in an independent cohort of TgSW172* mice.
[score:6]
These results indicated that pre-S/S-sW172* could upregulate miR-873 expression in at least two hepatoma cell lines (Hepa1-6 and HepY2).
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To understand whether the increased ER stress in transgenic mice was caused by pre-S/S-sW172* alone or also by miR-873 upregulation, the GRP78 levels were also compared between hepatoma cells with or without miR-873 overexpression.
[score:5]
The plasmid was generated based on a lentivirus expression vector, TOOLSilent shRNA Vector (TOOLS Biotechnology, New Taipei City, Taiwan), with insertion of a short stretch DNA sequence complementary to a target area of the miR-873 stem-loop sequence.
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Notably, in almost all cell lines (except for Huh7 and HepY2), miR-873 activation led to enhanced cell proliferation, consistent with the view that its target, CSMD3, was a tumor suppressor gene.
[score:5]
Finally, inhibition of miR-873 expression was achieved using a lentivirus -based vector in various hepatoma cell lines.
[score:5]
Activation of miR-873 to target CSMD3 by pre-S/S-sW172* expression in hepatoma cell linesTo further clarify the regulation cascade, pTg-sW172* was transfected into BNL, Hepa1-6, HepY2, Huh7, J7, and Mahlavu cells and miR-873 was assayed 3 days after transfection.
[score:5]
Following miR-873 inhibition, the CSMD3 expression remained undetectable in these three cell lines.
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These results were consistent with the actual changes of CSMD3 protein levels upon miR-873 inhibition (Figure 3f) and overexpression (Figure 4a).
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Activation of miR-873 to target CSMD3 by pre-S/S-sW172* expression in hepatoma cell lines.
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Inhibition of microRNA-873 expression.
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Besides increased ER stress response and apoptosis, resulting in enhanced hepatocyte proliferation and turnover, a miR-873 -mediated downregulation of CSMD3 contributed partly to hepatocarcinogenesis.
[score:4]
Up-regulation of miR-873 was found in Hepa1-6 and HepY2 cells (Figure 4b).
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When examining the regulatory cascade from pre-S/S-sW172* to CSMD3 suppression, it was found that activation of miR-873 only occurred in Hepa1-6 and HepY2 cells, suggesting that other cellular factors were involved in this process.
[score:4]
Increasing levels of miR-873 upregulation were noted (Figure 4c).
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The efficiency of anti-miR-873 expression was also assessed for comparison (Figure 3g).
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It was found that overexpression of miR-873 led to enhanced cell proliferation in Mahlavu, J7, Hepa1-6 and BNL cells.
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CSMD3 was undetectable in J7 cells with or without miR-873 overexpression.
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To understand whether CSMD3 was an authentic target of miR-873, the 3′-UTR of CSMD3 gene was inserted into the 3′-UTR of a luciferase gene for miR-873 co-transfection experiments.
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The targeted sequence of miR-873 was 5'-AGGAGACTCACAAGTTCCTG C-3'.
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Subsequently, miR-873 could target at CSMD3 by binding to the 3′-UTR of its transcripts.
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The putative miR-873-5p recognition seed site in the CSMD 3'UTR were subjected to site-specific mutagenesis by QuikChange Multi Site-Directed Mutagenesis Kit (Agilent Technologies, Santa Clara, CA, USA) (CSMD 3'UTR mut), and the mutated sequences were validated via automated DNA sequencing.
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For measuring the miRNA expression level from cells transfected with antisense miR-873-5p or miR-873 mimics, the ΔCt value was used to calculate expression levels normalized against U6 RNA.
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To examine the effects of miR-873 on CSMD3 3'UTR, the pMIR-CSMD3-3'UTR (wt or mut) was co -transfected with pre-miR-873 or mock control vector into hepatoma cells.
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As such, the increased ER stress in transgenic mice not only caused by pre-S/S-sW172* accumulation but also by miR-873 activation.
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Only microRNA-211 and micriRNA-873 (miR-873) satisfied these criteria.
[score:1]
To further clarify the regulation cascade, pTg-sW172* was transfected into BNL, Hepa1-6, HepY2, Huh7, J7, and Mahlavu cells and miR-873 was assayed 3 days after transfection.
[score:1]
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Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-195a, mmu-mir-30e, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-26a-1, mmu-mir-92a-2, mmu-mir-93, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-19b-1, mmu-mir-92a-1, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23b, rno-mir-25, rno-mir-26a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-98, rno-mir-103-2, rno-mir-103-1, rno-mir-106b, rno-mir-107, rno-mir-195, rno-mir-200c, rno-mir-221, rno-mir-223, mmu-mir-451a, rno-mir-451, mmu-mir-20b, rno-mir-20b, mmu-mir-711, mmu-mir-712, mmu-mir-713, mmu-mir-714, mmu-mir-717, mmu-mir-18b, mmu-mir-574, rno-mir-17-2, rno-mir-873, rno-mir-711, mmu-mir-195b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-873b, mmu-mir-451b, mmu-mir-30f, mmu-let-7k, rno-let-7g, rno-mir-15a
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment.
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Other miRNAs from this paper: mmu-mir-99b, mmu-mir-125a, mmu-mir-127, mmu-mir-9-2, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-19b-2, mmu-mir-26a-1, mmu-mir-351, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-376a, mmu-mir-381, mmu-mir-382, mmu-mir-383, mmu-mir-181b-2, mmu-mir-410, mmu-mir-433, mmu-mir-1224, mmu-mir-666, mmu-mir-873b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In the order of the significance score by SAM, 15 up-regulated miRNAs are mmu-miR-127, mmu-miR-410, mmu-miR-433, mmu-miR-138, mmu-miR-181c, mmu-miR-382, mmu-miR-19b, mmu-miR-381, mmu-miR-666-3p, mmu-miR-376a, mmu-miR-873, mmu-miR-181a, mmu-miR-383, mmu-miR-181b, and mmu-miR-99b.
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-27b, mmu-mir-124-3, mmu-mir-155, mmu-mir-10b, mmu-mir-186, mmu-mir-24-1, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-24-2, mmu-mir-1a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-375, mmu-mir-497a, mmu-mir-1b, mmu-mir-873b, mmu-mir-497b, mmu-mir-124b
Two miRNAs, miR-10b, and miR-873, were significantly downregulated in EtOHc-4D and AW8 neurons (data not shown).
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Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, mmu-mir-30b, mmu-mir-138-2, mmu-mir-143, hsa-mir-30b, hsa-mir-138-2, hsa-mir-143, hsa-mir-138-1, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-98, mmu-mir-148b, mmu-mir-342, mmu-mir-350, mmu-mir-135b, mmu-mir-17, mmu-mir-26a-2, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-362, mmu-mir-362, hsa-mir-376c, hsa-mir-342, hsa-mir-135b, hsa-mir-148b, mmu-mir-470, hsa-mir-490, mmu-mir-542, hsa-mir-487b, mmu-mir-376c, mmu-mir-487b, hsa-mir-574, hsa-mir-542, mmu-mir-744, mmu-mir-672, mmu-mir-674, mmu-mir-490, mmu-mir-466h, mmu-mir-574, hsa-mir-744, hsa-mir-873, mmu-mir-669j, mmu-mir-1930, mmu-mir-1934, mmu-mir-1942, mmu-mir-3064, mmu-mir-3065, mmu-mir-3069, mmu-mir-3071, mmu-mir-3073a, mmu-mir-3092, mmu-mir-3093, mmu-mir-3109, hsa-mir-3065, hsa-mir-3064, mmu-mir-3073b, mmu-mir-873b
01 Stress response, cell proliferation miR-542 ↓2.60 NA miR-574 ↑2.09 Inflammation (Tlr9 activation), cell proliferation, apoptosis miR-669j ↑3.12 NA miR-672 ↑2.40 NA miR-674 ↑2.19 NA miR-744 ↑4.35Oncogene (Tgf) suppression miR-873 ↑2.53 ↑3.22 NA miR-1930 ↑3.31 NA miR-1934 ↑2.17 ↑3.27 NA miR-1942 ↑2.49 NA miR-3064 ↑2.50 NA miR-3065 ↑3.20 NA miR-3069 ↑2.98 NA miR-3071 ↑3.51 NA miR-3073 ↓2.78 NA miR-3092 ↑3.48 NA miR-3093 ↑3.28 NA miR-3109 ↓2.07 NAAll reported variations were statistically significant (P < 0.05).
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Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-127, mmu-mir-128-1, mmu-mir-183, mmu-let-7d, 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-31, mmu-mir-128-2, mmu-mir-489, mmu-mir-485, mmu-mir-675, mmu-mir-673, mmu-mir-691, mmu-mir-707, mmu-mir-718, mmu-mir-875, mmu-mir-3064, mmu-mir-3074-1, mmu-mir-3074-2, mmu-let-7j, mmu-mir-873b, mmu-let-7k
miRNAs for Pik3cg (miR-707), Hbp1 (miR-127, miR-183, and miR-873), Twistnb (miR-718, and miR-691), and Dgkb (miR-489) had no impact on luciferase expression (Figure 2A and data not shown).
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-145a, mmu-mir-151, mmu-mir-181a-2, mmu-mir-184, mmu-mir-195a, mmu-mir-30e, mmu-mir-301a, mmu-let-7d, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-208a, mmu-mir-15a, mmu-mir-21a, mmu-mir-22, mmu-mir-322, mmu-mir-148b, mmu-mir-1a-2, mmu-mir-100, mmu-mir-210, mmu-mir-181a-1, mmu-mir-222, mmu-mir-133a-2, mmu-mir-370, mmu-mir-448, mmu-mir-451a, mmu-mir-463, mmu-mir-546, mmu-mir-541, mmu-mir-449c, mmu-mir-499, mmu-mir-711, mmu-mir-721, mmu-mir-743b, mmu-mir-881, mmu-mir-883a, mmu-mir-883b, mmu-mir-147, mmu-mir-208b, mmu-mir-1b, mmu-mir-1195, mmu-mir-1927, mmu-mir-1933, mmu-mir-1943, mmu-mir-669o, mmu-mir-3067, mmu-mir-3074-1, mmu-mir-3102, mmu-mir-3074-2, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-5123, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-873b, mmu-mir-451b, mmu-mir-30f
86 miR-873-as 1,016 e-miR-743b-5p 23.75 miR-449c-as 515e-miR-715 || 69.35 miR-541-as 439 e-miR-881* 56.21 miR-148b-as 336 e-miR-370 97.41 miR-546-as 333 e-miR-3067 100 miR-3074-as 262 e-miR-448-5p 100miR-451-as ‡ 286 e-miR-669o-5p 99.35 † Novel miR* that are processed within the expected window of the mature strand are labelled “generic”.
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