human tscc cell lines cal27  (ATCC)

Journal: Animal Models and Experimental Medicine

Article Title: The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

doi: 10.1002/ame2.12444

Figure Lengend Snippet: Relationship between Claudin‐1 expression and clinical characteristics of TSCC.

Article Snippet: Human TSCC cell lines SCC9 and Cal27 were procured from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Expressing

Journal: Animal Models and Experimental Medicine

Article Title: The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

doi: 10.1002/ame2.12444

Figure Lengend Snippet: Adenosine monophosphate–activated protein kinase (AMPK) activation can increase Claudin‐1 expression in a time‐dependent manner. The expression of phosphorylated‐AMPK (p‐AMPK), t‐AMPK, and Claudin‐1 in SCC9 cells after treatment with 0.5, 1, or 2 mmol/L 5‐aminoimidazole‐4‐carboxamide1‐β‐ d ‐ribofuranoside (AICAR) for 24 h (A–C) and 48 h (D–F). SCC9 cells were treated with 1 mmol/L AICAR for a short time for 10, 30, 60, and 90 min (G–I) and a long time for 24 and 48 h (J–L). The expression of p‐AMPK, t‐AMPK, and Claudin‐1 in Cal27 cells after treatment with 0.5, 1, or 2 mmol/L AICAR for 24 h (M–O) and 48 h (P–R). Cal27 cells were treated with 1 mmol/L AICAR for a short time for 10, 30, 60, and 90 min (S–U) and a long time for 24 h and 48 h (V–X). The protein expression was determined through western blotting, with glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) serving as the normalized control. Data are presented as the mean ± standard deviation from three independent experiments. ns, not significant; * p < 0.05; ** p < 0.01; and *** p < 0.001.

Article Snippet: Human TSCC cell lines SCC9 and Cal27 were procured from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Activation Assay, Expressing, Western Blot, Control, Standard Deviation

Journal: Animal Models and Experimental Medicine

Article Title: The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

doi: 10.1002/ame2.12444

Figure Lengend Snippet: Adenosine monophosphate–activated protein kinase (AMPK) activation can induce Claudin‐1 membranous translocation in a time‐dependent manner. The distribution of Claudin‐1 was examined using immunofluorescence in SCC9 cells treated with 1 mmol/L AICAR for short durations of 10, 30, 60, and 90 min with the same field of view at multiple magnifications (A) and for a longer duration of 24 h (B). Representative images of Claudin‐1 for short‐time treatment (red staining), 24 h treatment (green staining), and their semi‐quantitative results are shown (C, D). Bar = 15, 25, and 75 μm. ns, not significant; ** p < 0.01; and *** p < 0.001.

Article Snippet: Human TSCC cell lines SCC9 and Cal27 were procured from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Activation Assay, Translocation Assay, Immunofluorescence, Staining

Journal: Animal Models and Experimental Medicine

Article Title: The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

doi: 10.1002/ame2.12444

Figure Lengend Snippet: Activation of adenosine monophosphate–activated protein kinase (AMPK) inhibits the epithelial–mesenchymal transition (EMT) of tongue squamous cell carcinoma cells. The expression of EMT‐related proteins, namely E‐cadherin, β‐catenin, N‐cadherin, and vimentin, was detected by western blotting after 5‐aminoimidazole‐4‐carboxamide1‐β‐ d ‐ribofuranoside (AICAR, 1 mmol/L) treatment for 24 h in SCC9 cells (A–E), and Cal27 cells (F–J). Glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) was used as the normalized control. Data are presented as the mean ± standard deviation from three independent experiments. * p < 0.05; ** p < 0.01; and *** p < 0.001.

Article Snippet: Human TSCC cell lines SCC9 and Cal27 were procured from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Activation Assay, Expressing, Western Blot, Control, Standard Deviation

Journal: Animal Models and Experimental Medicine

Article Title: The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin‐1 via epithelial–mesenchymal transition

doi: 10.1002/ame2.12444

Figure Lengend Snippet: Knockdown of Claudin‐1 promoted the epithelial–mesenchymal transition (EMT) and migration of SCC9 cells. (A, B) The protein expression of Claudin‐1 in SCC9 cells transfected with short hairpin RNAs (shRNAs; namely sh1, sh2, and sh3) for 72 h was detected by western blotting. (C, D) Cell migration was assessed through the wound healing assay after incubation with or without 5‐aminoimidazole‐4‐carboxamide1‐β‐D‐ribofuranoside (AICAR, 1 mmol/L) for 48 h in Claudin‐1 stable knockdown cells transfected with Claudin‐1 shRNA (sh2 or sh3) and parent SCC9 cells. The relative migration effect of the cells was measured by the mean wound healing area. Data are presented as the mean ± standard deviation of four separate fields from three independent experiments. * p < 0.05; ** p < 0.01; and *** p < 0.001. (E–J) The EMT‐related protein expression in Claudin‐1 stable knockdown cell lines was detected by western blotting. All the results of western blotting are represented by three independent experiments. Glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) was used as the normalized control. shCon, negative control; ns, not significant; * p < 0.05; ** p < 0.01; and *** p < 0.001.

Article Snippet: Human TSCC cell lines SCC9 and Cal27 were procured from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Knockdown, Migration, Expressing, Transfection, Western Blot, Wound Healing Assay, Incubation, shRNA, Standard Deviation, Control, Negative Control