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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated <t>miRNA</t> enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology
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(A) and (B) RB slightly inhibited expression of p65 in PC3 and DU145 cells, while significantly for the Ser-536 phosphorylation of p65 ( p–p65 ), in both dosage-dependent and time-dependent manner. Lysates from whole cells treated with RB of different concentrations for 24 h (A) or with 10 µM RB for indicated times were used for western blot (B). GAPDH served as the loading control. Protein amount was normalized to the amount of GAPDH, and was quantified by densitometry of X-ray films. Results of one of at least three independent experiments are shown. (C) and (D) RB moderately down-regulated p65 mRNA level in PC3 and DU145 cells as detected by <t>QRT-PCR</t> assay. The procedure was performed as described in Materials and Methods . Results shown are representatives of three independent experiments, p<0.05 (*), versus RB-untreated control group respectively.
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Image Search Results


Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated miRNA enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology

Journal: Journal of translational medicine

Article Title: Identification of invasion-metastasis associated MiRNAs in gallbladder cancer by bioinformatics and experimental validation.

doi: 10.1186/s12967-022-03394-8

Figure Lengend Snippet: Fig. 2 GO functions for the target genes of the up-regulated and down-regulated miRNAs. A Up-regulated miRNA enriched biological process. B Up-regulated miRNAs enriched cellular component. C Up-regulated miRNAs enriched molecular function. D Down-regulated miRNAs enriched biological process. E Down-regulated miRNAs enriched cellular component. F Down-regulated miRNAs enriched molecular function. GO gene ontology

Article Snippet: All-in-OneTM miRNA qRTPCR Detection Kit (GeneCopoeia, USA) or Hifair® II 1st Strand cDNA Synthesis SuperMix (Yeasen, China) were used to make complementary DNA from 1 μg of RNA. qRT-PCR was performed using a LightCycler® 480 (Roche Molecular Systems, Inc., USA).

Techniques:

Fig. 3 The distribution of target genes of four selected miRNAs of different expression in GO-enriched functions. A Up-regulated miRNAs and (B) down-regulated miRNAs. Symbols of target genes were displayed on the left side of the graph. Gene involvement under GO terms was established by the colored connecting lines to the right. GO gene ontology. *P < 0.05; **P < 0.01

Journal: Journal of translational medicine

Article Title: Identification of invasion-metastasis associated MiRNAs in gallbladder cancer by bioinformatics and experimental validation.

doi: 10.1186/s12967-022-03394-8

Figure Lengend Snippet: Fig. 3 The distribution of target genes of four selected miRNAs of different expression in GO-enriched functions. A Up-regulated miRNAs and (B) down-regulated miRNAs. Symbols of target genes were displayed on the left side of the graph. Gene involvement under GO terms was established by the colored connecting lines to the right. GO gene ontology. *P < 0.05; **P < 0.01

Article Snippet: All-in-OneTM miRNA qRTPCR Detection Kit (GeneCopoeia, USA) or Hifair® II 1st Strand cDNA Synthesis SuperMix (Yeasen, China) were used to make complementary DNA from 1 μg of RNA. qRT-PCR was performed using a LightCycler® 480 (Roche Molecular Systems, Inc., USA).

Techniques: Expressing

Fig. 4 The regulatory network between dysregulated miRNAs and hub genes. A Up-regulated miRNAs and (B) down-regulated miRNAs. The mRNA expression of predicted targets for miRNAs were from the TCGA database. C MiR-642a-3p: SYK expression, SH3GL1 expression, CDKN1A expression. D MiR-145-5p: MYC expression, VEGFA expression, EGFR expression. *P < 0.05

Journal: Journal of translational medicine

Article Title: Identification of invasion-metastasis associated MiRNAs in gallbladder cancer by bioinformatics and experimental validation.

doi: 10.1186/s12967-022-03394-8

Figure Lengend Snippet: Fig. 4 The regulatory network between dysregulated miRNAs and hub genes. A Up-regulated miRNAs and (B) down-regulated miRNAs. The mRNA expression of predicted targets for miRNAs were from the TCGA database. C MiR-642a-3p: SYK expression, SH3GL1 expression, CDKN1A expression. D MiR-145-5p: MYC expression, VEGFA expression, EGFR expression. *P < 0.05

Article Snippet: All-in-OneTM miRNA qRTPCR Detection Kit (GeneCopoeia, USA) or Hifair® II 1st Strand cDNA Synthesis SuperMix (Yeasen, China) were used to make complementary DNA from 1 μg of RNA. qRT-PCR was performed using a LightCycler® 480 (Roche Molecular Systems, Inc., USA).

Techniques: Expressing

(A) and (B) RB slightly inhibited expression of p65 in PC3 and DU145 cells, while significantly for the Ser-536 phosphorylation of p65 ( p–p65 ), in both dosage-dependent and time-dependent manner. Lysates from whole cells treated with RB of different concentrations for 24 h (A) or with 10 µM RB for indicated times were used for western blot (B). GAPDH served as the loading control. Protein amount was normalized to the amount of GAPDH, and was quantified by densitometry of X-ray films. Results of one of at least three independent experiments are shown. (C) and (D) RB moderately down-regulated p65 mRNA level in PC3 and DU145 cells as detected by QRT-PCR assay. The procedure was performed as described in Materials and Methods . Results shown are representatives of three independent experiments, p<0.05 (*), versus RB-untreated control group respectively.

Journal: PLoS ONE

Article Title: Retigeric Acid B Exhibits Antitumor Activity through Suppression of Nuclear Factor-κB Signaling in Prostate Cancer Cells in Vitro and in Vivo

doi: 10.1371/journal.pone.0038000

Figure Lengend Snippet: (A) and (B) RB slightly inhibited expression of p65 in PC3 and DU145 cells, while significantly for the Ser-536 phosphorylation of p65 ( p–p65 ), in both dosage-dependent and time-dependent manner. Lysates from whole cells treated with RB of different concentrations for 24 h (A) or with 10 µM RB for indicated times were used for western blot (B). GAPDH served as the loading control. Protein amount was normalized to the amount of GAPDH, and was quantified by densitometry of X-ray films. Results of one of at least three independent experiments are shown. (C) and (D) RB moderately down-regulated p65 mRNA level in PC3 and DU145 cells as detected by QRT-PCR assay. The procedure was performed as described in Materials and Methods . Results shown are representatives of three independent experiments, p<0.05 (*), versus RB-untreated control group respectively.

Article Snippet: QRT-PCR was performed using the Eppendorf QRT-PCR System.

Techniques: Expressing, Western Blot, Quantitative RT-PCR

(A) RB dosage-dependently inhibited the mRNA expression of Bcl-x L , Bcl-2, survivin, and cyclin D1 as analyzed by QRT-PCR. GAPDH was used for normalization. Results are the mean ± SD of three independent experiments, each performed in triplicate. p<0.05 (*), p<0.01 (**), p<0.001 (***) versus RB-untreated control group respectively. (B) RB dosage-dependently inhibited expression of Bcl-x L , Bcl-2, survivin, and cyclin D. The results of western blot analysis of whole cell lysates from PC3 cells treated with different doses of RB were shown; GAPDH was included as a loading control. (C) RB inhibited invasion of PCa cells in a concentration-dependently manner as detected by transwell assay, (scale bar, 100 μm). The procedure was described in Materials and Methods . (D) The number of cells that invade through matrigel.

Journal: PLoS ONE

Article Title: Retigeric Acid B Exhibits Antitumor Activity through Suppression of Nuclear Factor-κB Signaling in Prostate Cancer Cells in Vitro and in Vivo

doi: 10.1371/journal.pone.0038000

Figure Lengend Snippet: (A) RB dosage-dependently inhibited the mRNA expression of Bcl-x L , Bcl-2, survivin, and cyclin D1 as analyzed by QRT-PCR. GAPDH was used for normalization. Results are the mean ± SD of three independent experiments, each performed in triplicate. p<0.05 (*), p<0.01 (**), p<0.001 (***) versus RB-untreated control group respectively. (B) RB dosage-dependently inhibited expression of Bcl-x L , Bcl-2, survivin, and cyclin D. The results of western blot analysis of whole cell lysates from PC3 cells treated with different doses of RB were shown; GAPDH was included as a loading control. (C) RB inhibited invasion of PCa cells in a concentration-dependently manner as detected by transwell assay, (scale bar, 100 μm). The procedure was described in Materials and Methods . (D) The number of cells that invade through matrigel.

Article Snippet: QRT-PCR was performed using the Eppendorf QRT-PCR System.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Concentration Assay, Transwell Assay