Abstract 3593: GABA counteracts ethanol induced stimulation of pancreatic cancer cells and normal pancreatic duct epithelia .

2013 ◽  
Author(s):  
Mohammed H. Al-Wadei ◽  
Hussein A.N. Al-Wadei ◽  
Hildegard M. Schuller
Keyword(s):  
Pancreatic Cancer ◽  
Pancreatic Duct ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
Stimulation Of

scholarly journals Activated Pancreatic Stellate Cells Enhance the Warburg Effect to Cause the Malignant Development in Chronic Pancreatitis

2021 ◽  
Author(s):  
Tao Ye ◽  
Shao Feng ◽  
Liu Zheng ◽  
Cai Ming ◽  
Meng Futao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Epithelial Cells ◽  
Pancreatic Duct ◽  
Cancer Cells ◽  
Stellate Cells ◽  
Glycolytic Enzymes ◽  
Pancreatic Stellate Cells ◽  
Migration And Invasion ◽  
Pancreatic Cancer Cells

Abstract Background: Chronic pancreatitis (CP) is a precancerous condition associated with pancreatic ductal adenocarcinoma (PDAC), but its evolutionary mechanism is unclear. pancreatic stellate cells (PSCs) are closely related to the occurrence and development of CP and PDAC. We aimed to find out whether PSCs play a key role in this " inflammationcancer transition ". Methods: To evaluate the effect of activated pancreatic stellate cells on normal pancreatic duct epithelial cells and pancreatic cancer cells, pancreatic stellate cells isolated from human tissues were co-cultured with these two cells, respectively. Functional assays assessed the proliferation, migration, and invasion of these two cells. RT-qPCR and western blotting were used to detect the mRNA and protein expressions of glycolytic enzymes in these two cells. Lactate production and glucose utilization assays assessed the aerobic glycolysis level of these two cells. Immunohistochemistry was used to detect the expression of glycolytic enzymes and α-SMA, and the correlation between the two was analyzed in human tissues. Results: Our research found that co-culture with activated PSCs promoted the proliferation, migration and invasion of normal pancreatic duct epithelial cells and pancreatic cancer cells. At the same time, activated PSCs had a significant effect on the expression of the glycolytic enzymes PKM2 and LDHA in normal pancreatic duct epithelial cells and pancreatic cancer cells and increased lactic acid production and glucose consumption in these two cells. In vivo experiments showed that the expression of the glycolytic enzymes PKM2 and LDHA in pancreatic duct epithelial cells and the marker protein (α-SMA) of activated PSCs in the pancreatic duct peripancreatic interstitium were higher in pancreatic cancer tissues and chronic pancreatitis tissues than in normal pancreatic tissues in both animals and humans. In addition, analysis of human tissue specimens showed that there is a correlation between the expression of PKM2/LDHA and α-SMA. Conclusion: These findings indicate that activated PSCs play an important role in the development and progression of chronic pancreatitis into pancreatic cancer by regulating and promoting aerobic glycolysis. Our research provides a new theoretical basis for further understanding the mechanism of CP malignancy and the selection of targets for reversing CP malignancy.

scholarly journals Schwann Cell Stimulation of Pancreatic Cancer Cells: A Proteomic Analysis

2020 ◽  
Vol 10 ◽  
Author(s):  
Aysha Ferdoushi ◽  
Xiang Li ◽  
Nathan Griffin ◽  
Sam Faulkner ◽  
M. Fairuz B. Jamaluddin ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Schwann Cell ◽  
Cancer Cells ◽  
Proteomic Analysis ◽  
Cell Stimulation ◽  
Pancreatic Cancer Cells ◽  
Stimulation Of

scholarly journals Activated Pancreatic Stellate Cells Enhance the Warburg Effect to Cause the Malignant Development in Chronic Pancreatitis

2021 ◽  
Author(s):  
Tao Ye ◽  
Shao Feng ◽  
Liu Zheng ◽  
Cai Ming ◽  
Meng Futao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Epithelial Cells ◽  
Pancreatic Duct ◽  
Cancer Cells ◽  
Stellate Cells ◽  
Monocarboxylate Transporter ◽  
Pancreatic Stellate Cells ◽  
Glucose Transporter 1 ◽  
Pancreatic Cancer Cells

Abstract Chronic pancreatitis (CP) is a precancerous condition associated with pancreatic ductal adenocarcinoma (PDAC), but its evolutionary mechanism is unclear. Pancreatic stellate cells (PSCs) are closely related to the occurrence and development of CP and PDAC, but it is not clear whether PSCs play a key role in this "inflammation-cancer transition". Our research found that co-culture with activated PSCs promoted the proliferation, migration and invasion of normal pancreatic duct epithelial cells and pancreatic cancer cells. At the same time, activated PSCs had a significant effect on the expression of the glycolysis markers (pyruvate kinase M2, lactate dehydrogenase A, glucose transporter 1, hexokinase-II and monocarboxylate transporter 4; PKM2, LDHA, GLUT1, HK2 and MCT4) in normal pancreatic duct epithelial cells and pancreatic cancer cells and increased lactic acid production and glucose consumption in these two cells. In vivo experiments showed that the expression of the glycolysis markers in pancreatic duct epithelial cells and the marker protein (α-SMA) of activated PSCs in the pancreatic duct peripancreatic interstitium were higher in pancreatic cancer tissues and chronic pancreatitis tissues than in normal pancreatic tissues in both animals and humans. In addition, analysis of human tissue specimens showed that there is a correlation between the expression of glycolysis markers and α-SMA. These findings indicate that activated PSCs play an important role in the development and progression of chronic pancreatitis into pancreatic cancer by regulating and promoting aerobic glycolysis. Our research provides a new theoretical basis for further understanding the mechanism of CP malignancy and the selection of targets for reversing CP malignancy.

scholarly journals The Relevance of Nrf2 Pathway and Autophagy in Pancreatic Cancer Cells upon Stimulation of Reactive Oxygen Species

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Lun Zhang ◽  
Jiahui Li ◽  
Jiguang Ma ◽  
Xin Chen ◽  
Ke Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Autophagic Flux ◽  
Oxygen Species ◽  
Nrf2 Pathway ◽  
Pancreatic Cancer Cells ◽  
Pathway Activation ◽  
Stimulation Of

Nrf2 (NF-E2-related factor 2) pathway and autophagy both can respond to oxidative stress to promote cancer cells to survive in the tumor microenvironment. We, therefore, explored the relevance between Nrf2 pathway and autophagy in pancreatic cancer cells upon stimulation of reactive oxygen species (ROS). Pancreatic cancer cells were cultured under controlled ROS stressing condition or basal condition. Different inhibitors were used to prevent autophagy at particular stages. Nrf2 siRNA was used to inhibit Nrf2 pathway activation. Ad-mRFP-GFP-LC3 infection was used to monitor autophagic flux. The result shows that a small amount of exogenous hydrogen peroxide (H2O2) can significantly improve the level of intracellular ROS. Moreover, our findings indicate that ROS promotes the activation of both Nrf2 pathway and autophagy in pancreatic cancer cells. Moreover, our data demonstrate that suppression of autophagic activity at particular stages results in an increased promotion of Nrf2 pathway activation upon ROS stimulation. Furthermore, we found that silencing of Nrf2 promotes autophagy upon ROS stimulation. In addition, Nrf2 interference effectively promotes autophagic flux upon ROS stimulation. In summary, our findings suggest that Nrf2 pathway and autophagy have a negative interaction with each other upon ROS stimulation.

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