Journal: Journal of Nanobiotechnology

Article Title: Selenium nanoparticles produce a beneficial effect in psoriasis by reducing epidermal hyperproliferation and inflammation

doi: 10.1186/s12951-021-00842-3

Figure Lengend Snippet: SeNPs inhibit the keratinocyte proliferation and epidermal hyperplasia. a–h Cells and i–p Mice were treated with SeNPs with various concentrations and protein was extracted to evaluate the protein expression. Ki67, Cyclin D1, PCNA, and mTOR proteins and phosphorylation of Akt, STAT3, and GSK3β was determined by Immunoblotting. Data represents Mean ± SD (in vitro n = 3; in vivo n = 5). *p < 0.05, ***p < 0.001, and ****p < 0.0001 are significantly different from the normal control group; ^^p < 0.01, ^^^p < 0.001, and ^^^^p < 0.0001 are significantly different from the EGF and IMQ groups

Article Snippet: The primary antibodies such as anti-p-MAPK p44/42, anti-MAPK p44/42, anti-p-SAPK/JNK, anti-SAPK/JNK, anti-p-MAPK p38, anti-MAPK p38, anti-p-GSK-3β, anti-GSK-3β, anti-p-Akt, anti-Akt, and anti-Cyclin D1 were purchased from Cell Signaling Technologies, USA.

Techniques: Expressing, Western Blot, In Vitro, In Vivo

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: Comparative analysis of VEGR2 and CD34 expressions in HCC tissues with different liver stiffness backgrounds. A. The expression levels of CD34 and VEGFR2 in HCC tissues with normal liver stiffness background, medium liver stiffness background and high liver stiffness background. B. A comparative analysis of the average IOD value of CD34 and VEGFR2 expression in three groups of HCC tissues with different liver stiffness backgrounds by image pro-plus 6.0 software. In each case, error bars represent SD, *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing, Software

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: Increased matrix stiffness actives AKT/Sp1 pathway and upregulates the expressions of VEGFR2 in HUVECs. A. mRNA expression level of VEGFR2 in HUVECs grown on 6 kPa stiffness substrate (L), 10 kPa stiffness substrate (M) and 16 kPa stiffness substrate (H). B. Protein expression level of VEGFR2 in HUVECs grown on 6 kPa stiffness substrate (L), 10 kPa stiffness substrate (M) and 16 kPa stiffness substrate (H). C. Higher matrix stiffness obviously elevates phosphorylation level of Akt in HUVECs. D. Higher matrix stiffness remarkably increased the expression of transcription factors Sp1 in HUVECs. E. Dual luciferase assay reveals an interaction between Sp1 and the promoter of gene VEGFR2.

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing, Luciferase

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: Integrin αV/β5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in HUVECs. A. Analysis of integrin subtypes in HUVECs under different stiffness stimulation. B. Antagonist SB273005 suppresses the phosphorylation level of Akt and VEGFR2 expression in HUVECs grown on 16 kPa stiffness substrate (H). C, D. siRNA against integrin αV or integrin β5 partially reverses the phosphorylation level of Akt and VEGFR2 expression in HUVECs grown on 16 kPa stiffness substrate (H). E. PI3K inhibitor LY294002 downregulates the phosphorylation level of Akt and the expressions of VEGFR2 and nuclear Sp1 in HUVECs grown on 16 kPa stiffness substrate (H).

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: VEGFR2 and CD34 expressions in TCGA-HCC tissues and their correlation with matrix stiffness. A. We defined the median expression of COL1A1 and LOX in TCGA-HCC tissues as the threshold to classify HCC patients into LOXhigh/COL1A1high group (45 patients) and LOXlow/COL1A1low group (44 patients), The mRNA expression level of VEGFR2 in TCGA-HCC tissues in LOXhigh/COL1A1high group (n=45) is obviously higher than that in LOXlow/COL1A1low group (n=44). B and C. Pearson correlation analysis indicates that the mRNA level of VEGFR2 in TCGA-HCC cohort is positively correlated with the mRNA level of COL1A1, while uncorrelated with that of LOX. D. The expression level of CD34 in HCC tissues LOXhigh/COL1A1high group (n=45) is significantly higher than that in LOXlow/COL1A1low group (n=44). E and F. Pearson correlation analysis indicates that the mRNA level of CD34 in TCGA-HCC cohort is positively correlated with that of both COL1A1 and LOX. **P<0.01, ****P<0.0001.

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: Associations of VEGFR2 expression with clinicopathologic characteristics in HCC patients

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: Correlation analysis between liver matrix stiffness and the VEGFR2/CD34 expression in HCC tissues. A. VEGFR2 and CD34 all exhibit obviously higher expression in LOXhigh/COL1A1high group compared to in LOXlow/COL1A1low group. ****P<0.0001. B. Representative images of immunohistochemistry staining of COL1A1, LOX, VEGFR2 and CD34.

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing, Immunohistochemistry, Staining

Journal: American Journal of Cancer Research

Article Title: Integrin αVβ5/Akt/Sp1 pathway participates in matrix stiffness-mediated effects on VEGFR2 upregulation in vascular endothelial cells

doi:

Figure Lengend Snippet: The proposed mechanism by which matrix stiffness upregulates the expression of VEGFR2 in HUVECs via activating integrin αVβ5/Akt/Sp1 pathway.

Article Snippet: Primary antibodies were diluted with 3% TBSA as follows: VEGFR2 (1:1000, Cell Signal Technology), Akt (1:1000, Cell Signal Technology), p-Akt (Ser473) (1:1000, Cell Signal Technology), Sp1 (1:1000, Cell Signal Technology), Integrin antibody sampler Kit (1:1000, Cell Signal Technology) and GAPDH (1:1000, Cell Signal Technology).

Techniques: Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: PRMT5 promotes epithelial‐mesenchymal transition via EGFR‐β‐catenin axis in pancreatic cancer cells

doi: 10.1111/jcmm.14894

Figure Lengend Snippet: PRMT5 activates EGFR/AKT/β‐catenin signalling in pancreatic cancer cells. A, Wnt/β‐catenin and EGFR signalling relative proteins were detected by Western blot in PaTu8988 and SW1990 sh‐PRMT5 stable infected cells. B, After transfected with pHA‐Venus or pHA‐PRMT5 plasmid in PaTu8988 and SW1990 sh‐PRMT5 stable infected cells, EGFR/AKT/β‐catenin signalling relative proteins were detected by Western blot. C, Pancreatic cancer cells were treated with EGFR inhibitor at 0, 10 μmol/L for 3 d. The expression of EGFR, p‐EGFR (Y1068) and PRMT5 was determined by Western blotting. D, The quantification of EGFR and p‐EGFR is shown. ** P < .01, *** P < .001. E, Wnt/β‐catenin and EGFR signalling relative proteins were detected by Western blot in PaTu8988 and SW1990 pHA‐PRMT5 stable infected cells treated with Erlotinib (10 μmol/L) for 3 d

Article Snippet: The following antibodies were used: PRMT5, β‐tubulin, collagen I (Abcam), E‐cadherin, Vimentin, β‐catenin, p‐EGFR (Y1068), EGFR, (Cell Signaling Technology), Akt, p‐Akt, GSK‐3β, p‐GSK‐3β, p‐EGFR (Y1172), HA (ImmunoWay) and HRP‐conjugated secondary antibodies (Pierce).

Techniques: Western Blot, Infection, Transfection, Plasmid Preparation, Expressing