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In the materials industry, it is significant to clarify the correlation between material dispersion morphology and the mechanical properties of rubber blends, which are comprehensively employed and are always in...

Introduction: Pancreatic adenocarcinoma (PAAD) is a lethal cancer, and metabolic reprogramming in PAAD is a clinical concern. The RAS oncogene family member RAB10 is highly expressed in many tumor tissues, but its role in PAAD remains unclear. Here, we explore correlations between RAB10 expression and PAAD prognosis. We investigate whether RAB10 regulates glucose uptake in PAAD cells through modulating the expression and location of the glucose transporter (GLUT1).Methods: Immunohistochemical staining was used to detect the expression of RAB10 in pancreaticoduodenectomy specimens. The function of PAAD cells expressing different levels of RAB10 was assessed by CCK-8 proliferation, wound healing, and transwell migration assays. Glucose uptake assays and lactate production assays were used to explore the effects of RAB10 on PAAD cell metabolism. In addition, we used qRT-PCR, western blot, and immunofluorescence to analyze interactions between RAB10 and GLUT members.Results: RAB10 was highly expressed in PAAD tissues and cell lines, and was significantly correlated with T classification and pathological differentiation. High RAB10 expression was found to be an independent prognostic factor of poor disease outcomes in PAAD. RAB10 knockdown inhibited proliferation, invasion, and metastasis of PAAD cells, and downregulated glucose uptake and lactate production. Down-regulation of RAB10 inhibited GLUT1 translocating to the cell membrane and downregulated GLUT1 expression, which in turn decreased glucose uptake in tumor cells.Conclusion: These results demonstrate that overexpression of RAB10 is associated with worse PAAD survival outcomes. Downregulation of RAB10 may decrease glucose uptake in tumor cells by inhibiting GLUT1 membrane localization and downregulating GLUT1 expression.

Introduction: Pancreatic adenocarcinoma (PAAD) is a lethal cancer, and metabolic reprogramming in PAAD is a clinical concern. The RAS oncogene family member RAB10 is highly expressed in many tumor tissues, but its role in PAAD remains unclear. Here, we explore correlations between RAB10 expression and PAAD prognosis. This study investigated whether RAB10 regulates glucose uptake in PAAD cells through modulating the expression and location of the glucose transporter1 (GLUT1).Methods: Immunohistochemical staining was used to detect the expression of RAB10 in pancreaticoduodenectomy specimens. The function of PAAD cells expressing different levels of RAB10 was assessed by CCK-8 proliferation, wound healing, and transwell migration assays. Glucose uptake assays and lactate production assays were used to explore the effects of RAB10 on PAAD cell metabolism. In addition, we used qRT-PCR, western blot, and immunofluorescence to analyze interactions between RAB10 and GLUT members.Results: RAB10 was highly expressed in PAAD tissues and cell lines, and was significantly correlated with T classification and pathological differentiation. High RAB10 expression was found to be an independent prognostic factor of poor disease outcomes in PAAD. RAB10 knockdown inhibited proliferation, invasion, and metastasis of PAAD cells, and downregulated glucose uptake and lactate production. Down-regulation of RAB10 inhibited GLUT1 translocating to the cell membrane and downregulated GLUT1 expression, which in turn decreased glucose uptake in tumor cells.Conclusion: These results demonstrate that overexpression of RAB10 is associated with worse PAAD survival outcomes. Downregulation of RAB10 may decrease glucose uptake in tumor cells by inhibiting GLUT1 membrane localization and downregulating GLUT1 expression.