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AIM: To investigate the expression of phosphor-rylated signal transduction and activators of transcription-3 (p-STAT3) and E-cadherin as well as their correlations with the clinicopathological parameters in pancreatic cancer, and to reveal the role of STAT3 signal pathway in the invasion and metastasis of pancreatic cancer. METHODS: Immunohistochemistry was used to detect the expression of p-STAT3 and E-cadherin in 34 cases of pancreatic cancer and 10 cases of normal pancreatic tissues. Cell invasion assay kit was used to examine the invasion ability of pancreatic cancer cells SW1990 and CaPan-2. Western blot and electrophoretic mobility shift assay (EMSA) were applied to detect the protein expression of p-STAT3 and STAT3 DNA-binding activity in SW1990 and CaPan-2 cells. RESULTS: Immunohistochemistry revealed high expression of p-STAT3 (64.7%) but low expression of E-cadherin in pancreatic cancer. The expression of p-STAT3 was significantly correlated with the clinical stages (P=0.017)
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AIM: To investigate the expression of phosphor-rylated signal transduction and activators of transcription-3 (p-STAT3) and E-cadherin as well as their correlations with the clinicopathological parameters in pancreatic cancer, and to reveal the role of STAT3 signal pathway in the invasion and metastasis of pancreatic cancer. METHODS: Immunohistochemistry was used to detect the expression of p-STAT3 and E-cadherin in 34 cases of pancreatic cancer and 10 cases of normal pancreatic tissues. Cell invasion assay kit was used to examine the invasion ability of pancreatic cancer cells SW1990 and CaPan-2. Western blot and electrophoretic mobility shift assay (EMSA) were applied to detect the protein expression of p-STAT3 and STAT3 DNA-binding activity in SW1990 and CaPan-2 cells. RESULTS: Immunohistochemistry revealed high expression of p-STAT3 (64.7%) but low expression of E-cadherin in pancreatic cancer. The expression of p-STAT3 was significantly correlated with the clinical stages (P=0.017)
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