Objective:To investigate the role of RASAL2 in vasculogenic mimicry in pancreatic cancer cells and to preliminarily explore the potential molecular mechanisms involved.Methods:The clinical proteomic tumor analysis consortium(CPTAC)database was used to analyze the expression of RASAL2 in pancreatic cancer,and immunohistochemical method was used to detect the expression of RASAL2,β-catenin and Vimentin in pancreatic cancer and adjacent tissues.In the pancreatic cancer cell line,after lentivirus infection knockdown and overexpression of RASAL2,transcriptome sequencing was performed on pancreatic cancer cells silencing RASAL2 expression,and vasculogenic mimicry experiment was used to detect the effect of RASAL2 on angiogenesis of pancreatic cancer cells;The molecular mechanism of RASAL2 promoting vasculogenic mimicry in pancreatic cancer was studied by real-time fluorescent quantitative PCR and Western blotting detection.Results:The analysis results of CPTAC database showed that the expression level of RASAL2 protein in pancreatic cancer tissue was significantly higher than that in normal pancreatic tissue.Immunohistochemical test results showed that the expression of RASAL2 in pancreatic cancer tissue was up-regulated,and the expression of β-catenin and Vimentin in pancreatic cancer tissue was also significantly up-regulated.The second-generation transcriptome sequencing results showed that RASAL2 may be involved in the biological behavior of intercellular connections and adhesion.After knocking down RASAL2 expression in pancreatic cancer cell PANC-1,the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins decreased,and the formation of vasculogenic mimicry structure was inhibited;After overexpression of RASAL2 in pancreatic cancer cell BxPC-3,the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins increased,promoting the formation of vasculogenic mimicry.Conclusion:The effect of RASAL2 on vasculogenic mimicry in pancreatic cancer cells is related to AKT/β-catenin signaling pathway.

Objective:To investigate the role of RASAL2 in vasculogenic mimicry in pancreatic cancer cells and to preliminarily explore the potential molecular mechanisms involved.Methods:The clinical proteomic tumor analysis consortium(CPTAC)database was used to analyze the expression of RASAL2 in pancreatic cancer,and immunohistochemical method was used to detect the expression of RASAL2,β-catenin and Vimentin in pancreatic cancer and adjacent tissues.In the pancreatic cancer cell line,after lentivirus infection knockdown and overexpression of RASAL2,transcriptome sequencing was performed on pancreatic cancer cells silencing RASAL2 expression,and vasculogenic mimicry experiment was used to detect the effect of RASAL2 on angiogenesis of pancreatic cancer cells;The molecular mechanism of RASAL2 promoting vasculogenic mimicry in pancreatic cancer was studied by real-time fluorescent quantitative PCR and Western blotting detection.Results:The analysis results of CPTAC database showed that the expression level of RASAL2 protein in pancreatic cancer tissue was significantly higher than that in normal pancreatic tissue.Immunohistochemical test results showed that the expression of RASAL2 in pancreatic cancer tissue was up-regulated,and the expression of β-catenin and Vimentin in pancreatic cancer tissue was also significantly up-regulated.The second-generation transcriptome sequencing results showed that RASAL2 may be involved in the biological behavior of intercellular connections and adhesion.After knocking down RASAL2 expression in pancreatic cancer cell PANC-1,the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins decreased,and the formation of vasculogenic mimicry structure was inhibited;After overexpression of RASAL2 in pancreatic cancer cell BxPC-3,the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins increased,promoting the formation of vasculogenic mimicry.Conclusion:The effect of RASAL2 on vasculogenic mimicry in pancreatic cancer cells is related to AKT/β-catenin signaling pathway.