Journal: Brazilian dental journal

Article Title: ING3 and ING4 immunoexpression and their relation to the development of benign odontogenic lesions.

doi: 10.1590/0103-6440202104279

Figure Lengend Snippet: Figure 1. Positive controls for ING3 and ING4 immunolabeling in specimens of oral squamous cell carcinoma (OSCC) and dental follicle. (A) ING3 expression in OSCC. (B) ING4 expression in OSCC. (C) ING3 expression in dental follicle. (D) ING4 expression in dental follicle (IHC; 100x magnification).

Article Snippet: Concerning ING4, a polyclonal antibody (clone NBP2-33828; Novus Biologicals) also used in a dilution of 1:4000, with the same specifications of antigenic recovery and incubation time as the previously mentioned antibody.

Techniques: Immunolabeling, Expressing

Journal: Brazilian dental journal

Article Title: ING3 and ING4 immunoexpression and their relation to the development of benign odontogenic lesions.

doi: 10.1590/0103-6440202104279

Figure Lengend Snippet: Figure 3. ING4 cytoplasmic and nuclear immunolabeling in AM, OKC and AOT. (A) Moderate cytoplasmic immunolabelling in AM. (B) Low nuclear expression in the epithelial component of AM. (C) OKC showing high cytoplasmic expression of ING4. (D) Absence of nuclear immunolabeling in the epithelial lining of OKC. (E)/(F) High cytoplasmic and nuclear immunolabeling in AOT tumor parenchyma cells (IHC)

Article Snippet: Concerning ING4, a polyclonal antibody (clone NBP2-33828; Novus Biologicals) also used in a dilution of 1:4000, with the same specifications of antigenic recovery and incubation time as the previously mentioned antibody.

Techniques: Immunolabeling, Expressing

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 1: Expression of p33ING1b and p29ING4 in renal cell carcinoma. (a) mRNA expression of p33ING1b and p29ING4 was increased at early and late stages of disease with higher expression of both genes at late stages of disease compared to early stages (Robson stages III/IV vs. I/II) (p33ING1b and p29ING4: stages I/II and III/IV vs. normal tissue p<0.001 and p<0.0001, respectively; p33ING1b and p29ING4: stages III/IV vs. I/II p<0.01 and p<0.001, respectively). (b) Results of the real time RT-PCR were normalized to kidney normal tissue and expressed as x-fold difference (2- ∆∆Ct). Expression of p33ING1b and p29ING4 by renal carcinoma cells was confirmed (Cy3 red; DAPI blue (nuclear counterstaining)). (c) Sections are representative of n=30 patients/group. Representative western blots of p33ING1b and p29ING4 (loading control ß-actin).

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 4: p33ING1b- and p29ING4-specific T cell reactivity. Four peptides resulted in significantly increased expression of IFN-γ compared to controls, independent of tumor stage (p33ING1b (aa109-118) and aa259-268, and p29ING4 (aa149-158) and aa239-248; p<0.001) Stages I/ II (a) and Stages III/IV (b). Elispot analysis was measured as spots/5 x 105 cells/patient.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Enzyme-linked Immunospot

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 5: p33ING1b- and p29ING4-specific T cell reactivity. Two peptides resulted in increased expression of IL-10 compared to controls; peptide p33ING1b (aa109-118) at all stages and p29ING4 (aa239-248) at late stages (p<0.001). Stages I/ II (a) and Stages III/IV (b). Luminex analysis was measured as pg/ml.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Luminex

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 6: p33ING1b- and p29ING4-specific T cell reactivity. Evaluation of IL-2 expression revealed that only a single epitope (p29ING4 (aa149-158)) resulted in high responsiveness of T cells from RCC patients after stimulation with the peptide (stages I/II vs. III/IV p<0.001). PBMCs from healthy volunteers (n=30) had no significant IL-2 expression after stimulation with all peptide epitopes. Luminex analysis for IL-2 expression was measured as pg/ml and presented as percent stimulation index.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Expressing, Luminex

Journal: Journal of Clinical & Cellular Immunology

Article Title: Tumor Suppressor Gene P29ing4 is Overexpressed and Induces a CD8 T Effector Cell Response in Human Renal Cell Carcinoma

doi: 10.4172/2155-9899.1000511

Figure Lengend Snippet: Figure 7: p29ING4 presentation by MHC class I (a) and II (b) molecules. p29ING4 presentation by major histocompatibility complex (MHC) class I and II antigens was shown to be increased in RCC but not in healthy kidneys.

Article Snippet: Analysis of single staining was performed for p33ING1 (Santa Cruz Biotechnology, CA, USA), p29ING4 (Rockland/Biomol, Hamburg, Germany) CD4, CD25, Foxp3, CD8, (Abcam, Cambridge, UK), IFN-γ (BD Pharmingen, Heidelberg, Germany), IL-2, and IL-10 (R&D Systems, Minneapolis, USA).

Techniques: Immunopeptidomics

Journal: Molecular medicine reports

Article Title: MicroRNA‑214 upregulates HIF‑1α and VEGF by targeting ING4 in lung cancer cells.

doi: 10.3892/mmr.2019.10170

Figure Lengend Snippet: Figure 3. miR‑214 regulates ING4, HIF‑1α, VEGF, AK3 and MMP2 protein expression. (A) Western blotting showed that miR‑214 mimic transfection significantly increased HIF‑1α, VEGF, AK3 and MMP2 protein expression levels, and significantly decreased ING4 expression in A549 and H1299 cell lines. HIF‑1α, MMP2, AK3 and VEGF expressions levels decreased, and ING4 expression increased in A549 and H1299 cells transfected with miR‑214 inhibitor. (B) Quantification of the western blotting results. *P<0.05 vs. mimic control; #P<0.05 vs. inhibitor control. ING4, inhibitor of growth family member 4; HIF‑1α, hypoxia‑inducible factor 1α; AK3, adenylate kinase 3; VEGF, vascular endothelial growth factor; MMP2, matrix metalloproteinase 2; miR‑214, microRNA‑214.

Article Snippet: The membranes were incubated overnight at 4 ̊C with primary antibodies against inG4 (1:800; cat. no. 10617-1-aP; ProteinTech Group, inc., chicago, il, uSa), adenylate kinase 3 (aK3; 1:800; cat. no. 12562-1-aP; ProteinTech Group, inc.), matrix metalloproteinase 2 (MMP2; 1:800; cat. no. 10373-2-aP; ProteinTech Group, inc.), HiF-1α (1:1,000; cat. no. ab51608; abcam, cambridge, Ma, uSa), VeGF (1:1,000; cat. no. ab53465ame; abcam) and GaPdH (1:2,000; cat. no. 2118; cell Signaling Technology, inc., danvers, Ma, uSa).

Techniques: Expressing, Western Blot, Transfection, Control

Journal: Molecular medicine reports

Article Title: MicroRNA‑214 upregulates HIF‑1α and VEGF by targeting ING4 in lung cancer cells.

doi: 10.3892/mmr.2019.10170

Figure Lengend Snippet: Figure 4. ING4 is a target of miR‑214. (A) RT‑qPCR demonstrated that miR‑214 mimics downregulated the mRNA expression of ING4 mRNA, whereas miR‑214 inhibitor had the opposite effect. (B) The luciferase reporter assay showed that in cells transfected with the wild‑type reporter, miR‑214 mimics significantly inhibited luciferase activity. In cells transfected with the mutant site reporter plasmid, no significant alteration was detected. (C) ING4 expression was examined by RT‑qPCR in 20 lung cancer cases. Linear regression analyses demonstrated that there was an inverse correlation between miR‑214 and ING4 mRNA expression levels. *P<0.05 vs. corresponding control. ING4, inhibitor of growth family member 4; miR‑214, microRNA‑214; RT‑qPCR, reverse transcription‑quantitative polymerase chain reaction.

Article Snippet: The membranes were incubated overnight at 4 ̊C with primary antibodies against inG4 (1:800; cat. no. 10617-1-aP; ProteinTech Group, inc., chicago, il, uSa), adenylate kinase 3 (aK3; 1:800; cat. no. 12562-1-aP; ProteinTech Group, inc.), matrix metalloproteinase 2 (MMP2; 1:800; cat. no. 10373-2-aP; ProteinTech Group, inc.), HiF-1α (1:1,000; cat. no. ab51608; abcam, cambridge, Ma, uSa), VeGF (1:1,000; cat. no. ab53465ame; abcam) and GaPdH (1:2,000; cat. no. 2118; cell Signaling Technology, inc., danvers, Ma, uSa).

Techniques: Expressing, Luciferase, Reporter Assay, Transfection, Activity Assay, Mutagenesis, Plasmid Preparation, Control, Polymerase Chain Reaction

Journal: Molecular medicine reports

Article Title: MicroRNA‑214 upregulates HIF‑1α and VEGF by targeting ING4 in lung cancer cells.

doi: 10.3892/mmr.2019.10170

Figure Lengend Snippet: Figure 5. ING4 overexpression upregulates MMP2, HIF‑1α and VEGF expression. (A) Western blotting confirmed that ING4 plasmid transfection upregulated ING4 protein expression in A549 and H1299 cells. (B) A549 and H1299 cells were transfected with the mimic control, miR‑214 mimics alone or together with the ING4 plasmid. ING4 plasmid re‑constituted its endogenous expression and downregulated MMP2, HIF‑1α and VEGF expression when compared with the groups transfected with miR‑214 mimic alone in A549 and H1299 cell lines. (C) Quantification of western blotting results. These experiments were performed in triplicate. *P<0.05 vs. control group; #P<0.05 vs. mimic group. ING4, inhibitor of growth family member 4; HIF‑1α, hypoxia‑inducible factor 1α; AK3, adenylate kinase 3; VEGF, vascular endothelial growth factor; MMP2, matrix metalloproteinase 2; miR‑214, microRNA‑214.

Article Snippet: The membranes were incubated overnight at 4 ̊C with primary antibodies against inG4 (1:800; cat. no. 10617-1-aP; ProteinTech Group, inc., chicago, il, uSa), adenylate kinase 3 (aK3; 1:800; cat. no. 12562-1-aP; ProteinTech Group, inc.), matrix metalloproteinase 2 (MMP2; 1:800; cat. no. 10373-2-aP; ProteinTech Group, inc.), HiF-1α (1:1,000; cat. no. ab51608; abcam, cambridge, Ma, uSa), VeGF (1:1,000; cat. no. ab53465ame; abcam) and GaPdH (1:2,000; cat. no. 2118; cell Signaling Technology, inc., danvers, Ma, uSa).

Techniques: Over Expression, Expressing, Western Blot, Plasmid Preparation, Transfection, Control

Journal: Molecular medicine reports

Article Title: MicroRNA‑214 upregulates HIF‑1α and VEGF by targeting ING4 in lung cancer cells.

doi: 10.3892/mmr.2019.10170

Figure Lengend Snippet: Figure 6. ING4 siRNA transfection downregulates MMP2, HIF‑1α and VEGF expression. (A) Western blotting confirmed that ING4 siRNA transfection downregulated ING4 protein expression in A549 and H1299 cells. (B) A549 and H1299 cells were transfected with the inhibitor control, miR‑214 inhibitor or miR‑214 inhibitor together with ING4 siRNA. ING4 siRNA downregulated MMP2, HIF‑1α and VEGF, which were induced by miR‑214. (C) Quantification of western blotting results. These experiments were performed in triplicate. **P<0.01 vs. control group; ##P<0.01 vs. mimic group. ING4, inhibitor of growth family member 4; HIF‑1α, hypoxia‑inducible factor 1α; AK3, adenylate kinase 3; VEGF, vascular endothelial growth factor; MMP2, matrix metalloproteinase 2; miR‑214, microRNA‑214.

Article Snippet: The membranes were incubated overnight at 4 ̊C with primary antibodies against inG4 (1:800; cat. no. 10617-1-aP; ProteinTech Group, inc., chicago, il, uSa), adenylate kinase 3 (aK3; 1:800; cat. no. 12562-1-aP; ProteinTech Group, inc.), matrix metalloproteinase 2 (MMP2; 1:800; cat. no. 10373-2-aP; ProteinTech Group, inc.), HiF-1α (1:1,000; cat. no. ab51608; abcam, cambridge, Ma, uSa), VeGF (1:1,000; cat. no. ab53465ame; abcam) and GaPdH (1:2,000; cat. no. 2118; cell Signaling Technology, inc., danvers, Ma, uSa).

Techniques: Transfection, Expressing, Western Blot, Control

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: MiR-761 Promotes Progression and Metastasis of Non-Small Cell Lung Cancer by Targeting ING4 and TIMP2.

doi: 10.1159/000430333

Figure Lengend Snippet: Fig. 6. ING4 and TIMP2 suppress NSCLC cell proliferation and motility. (A) Western blot of ING4 expression in H460 cells transfected with ING4 siRNA or scrambled siRNA. (B-D) MTT (B), wound healing (C), and transwell (D) assays in H460 cells transfected with ING4 siRNA or scrambled siRNA. (E) Western blot of ING4 expression in H460 cells transfected with TIMP2 siRNA or scrambled siRNA. (F-H) MTT (F), wound healing (G), and transwell (H) assays in H460 cells transfected with TIMP2 siRNA or scrambled siRNA. *p<0.05, **p<0.01 when compared to scrambled siRNA-transfected cells.

Article Snippet: MiRNA, siRNA, plasmids, and transfection MiR-761, miR-NC (miR-negative control), antimiR-761, antimiR-NC, ING4 siRNA, TIMP2 siRNA, and scrambled siRNA were all purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Western Blot, Expressing, Transfection