Journal: Experimental and Therapeutic Medicine

Article Title: Role of S100A3 in human hepatocellular carcinoma and the anticancer effect of sodium cantharidinate

doi: 10.3892/etm.2017.4294

Figure Lengend Snippet: Expression of S100A3 in human HCC tissues and HepG2 cells. (A) Immunohistochemical staining of S100A3 in human HCC tissues and (B) adjacent non-tumorous tissues, the red arrows indicate the S100A3-positive cells. S100A3 (C) protein and (D) mRNA expression levels in human adjacent non-tumorous tissue (control) compared with human HCC tissues (HCC), respectively. (E) Western blotting indicated the expression of S100A3 expressed in HepG2 cells and PHH. Data are expressed as the mean ± standard deviation of three experiments (***P<0.001 vs. control). HCC, hepatocellular carcinoma; S100A3, S100 calcium-binding protein A3; PHH, primary human hepatocytes.

Article Snippet: The membrane was blocked with 0.05% Tween-20 in PBS containing 5% skimmed milk and incubated overnight with the primary S100A3 antibody (WH0006274M1; 1:1,000; Sino Biological Inc., Beijing, China) at 4°C overnight.

Techniques: Expressing, Immunohistochemical staining, Staining, Western Blot, Standard Deviation, Binding Assay

Journal: Experimental and Therapeutic Medicine

Article Title: Role of S100A3 in human hepatocellular carcinoma and the anticancer effect of sodium cantharidinate

doi: 10.3892/etm.2017.4294

Figure Lengend Snippet: Effect of sodium cantharidinate on the expression of S100A3 in HepG2 cells. (A) S100A3 gene alteration of sodium cantharidinate-treated HepG2 cells compared with the control. (B and C) Western blotting was performed to indicate S100A3 protein expression levels in HepG2 cells. HepG2 cells were exposed to either control solution (0.1% DMSO in medium) or sodium cantharidinate (5.0 µM/l) and incubated for 48 h. Experiments were performed in triplicate. Data are expressed as the mean ± standard deviation of three experiments (***P<0.001 vs. control). S100A3, S100 calcium-binding protein A3.

Article Snippet: The membrane was blocked with 0.05% Tween-20 in PBS containing 5% skimmed milk and incubated overnight with the primary S100A3 antibody (WH0006274M1; 1:1,000; Sino Biological Inc., Beijing, China) at 4°C overnight.

Techniques: Expressing, Western Blot, Incubation, Standard Deviation, Binding Assay

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 9. HepG2.2.15 cell line treated with different concentrations of 16F16 drug. (A) Western blot analysis of the expression levels of S100A3 in hepG2.2.15 cells treated with 16F16, which were also consistent with the qPCR analysis, S100A3 is also downregulated at 4 μg/ mL concentration of 16F16 in western blot analysis. Asterisks indicate statistical signifi cance (*P < 0.05, **P < 0.01, ***P < 0.001). (B) qPCR analysis of the transcription of S100A3 in hepG2.2.15 cells treated with 16F16, it was shown that at 4 μg/mL concentration of 16F16 is effective in downregulating S100A3 transcript in HepG2.2.15 cell line. All experi ments were repeated three times.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Western Blot, Expressing, Concentration Assay

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 10. HepG2.2.15 treatment with S100A3-expressing plasmid pLVX-puro-S100A3. (A and B) HepG2.2.15 cell line was treated with pLVX-puro-S100A3, super natant was collected at different time intervals to elucidate effect of S100A3 upregulation on HBsAg and HBeAg, results indicated that S100A3 upregulation results in upregulation of HBsAg and HBeAg. (C) S100A3 also found to be effective in modulating HBV genome, HBV genome was also increased after pLVX-puro-S100A3 treatment in HepG2.2.15 cell line. (D) mRNA expression of S100A3, HBV DNA and HBsAg mRNA in HepG2.2.15 cells expressing the S100A3 gene by pLVX- puro-S100A3, determined using reverse transcription-quantitative polymerase chain reaction analysis. (E) Western blot analysis of HepG2.2.15 cell line after transfection with pLVX-puro-S100A3.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Expressing, Plasmid Preparation, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Transfection

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 11. S100A3 knockdown modulates secretion of HBV antigens and HBV DNA (A-B) S100A3-shRNA is used for knockdown the expression of S100A3, HBsAg and HBeAg were downregulated after treatment with shS100A3. (C) qPCR analysis showed that after S100A3 knock down mRNA levels of HBx and HBs proteins were significantly reduced as compared to control and HepG2.2.15 cells. (D) HBV DNA decreased after shS100A3 treatment in time dependent manner as compared to control and HepG2.2.15 cells, determined by using reverse transcription-quantitative polymerase chain reaction analysis. (E) Western blot analysis verified the successful knockdown of S100A3 in HepG2.2.15 cell line.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Knockdown, shRNA, Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot

Journal: Frontiers in Cell and Developmental Biology

Article Title: Hypoxia-immune-related microenvironment prognostic signature for osteosarcoma

doi: 10.3389/fcell.2022.974851

Figure Lengend Snippet: List of primers.

Article Snippet: Then, membranes were blocked with 5% w/v skim milk, incubated with primary antibodies against BNIP3 (1:1,000; 68091-1-Ig; Proteintech), SLC38A5 (1:1,000; 28102-1-AP; Proteintech), SLC5A3 (1:1,000; 21628-1-AP; Proteintech), CKMT2 (1:1,000; 13207-1-AP; Proteintech), S100A3 (1:1,000; 12343-1-AP; Proteintech), PGM1 (1:1,000; 15161-1-AP; Proteintech), CXCL11 (1:1,000; MAB672-SP; R&D Systems) and β-actin antibody (1:5,000; NB-600; Sigma) overnight at 4 °C.

Techniques: Sequencing