scholarly journals Pancreatic stellate cells are an important source of MMP-2 in human pancreatic cancer and accelerate tumor progression in a murine xenograft model and CAM assay

2007 ◽  
Vol 120 (3) ◽  
pp. 512-519 ◽  
Author(s):  
W. Schneiderhan ◽  
F. Diaz ◽  
M. Fundel ◽  
S. Zhou ◽  
M. Siech ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Progression ◽  
Xenograft Model ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreatic Cancer ◽  
Cam Assay ◽  
Murine Xenograft Model

scholarly journals Differential Gemcitabine Sensitivity in Primary Human Pancreatic Cancer Cells and Paired Stellate Cells Is Driven by Heterogenous Drug Uptake and Processing

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3628
Author(s):  
Manoj Amrutkar ◽  
Nils Tore Vethe ◽  
Caroline S. Verbeke ◽  
Monica Aasrum ◽  
Anette Vefferstad Finstadsveen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Stellate Cells ◽  
Drug Uptake ◽  
Pancreatic Stellate Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
The Impact

Gemcitabine resistance in pancreatic ductal adenocarcinoma (PDAC) is attributed to cancer cell-intrinsic drug processing and the impact of the tumor microenvironment, especially pancreatic stellate cells (PSCs). This study uses human PDAC-derived paired primary cancer cells (PCCs) and PSCs from four different tumors, and the PDAC cell lines BxPC-3, Mia PaCa-2, and Panc-1, to assess the fate of gemcitabine by measuring its cellular uptake, cytotoxicity, and LC-MS/MS-based metabolite analysis. Expression analysis and siRNA-mediated knockdown of key regulators of gemcitabine (hENT1, CDA, DCK, NT5C1A) was performed. Compared to PSCs, both the paired primary PCCs and cancer cell lines showed gemcitabine-induced dose-dependent cytotoxicity, high uptake, as well as high and variable intracellular levels of gemcitabine metabolites. PSCs were gemcitabine-resistant and demonstrated significantly lower drug uptake, which was not influenced by co-culturing with their paired PCCs. Expression of key gemcitabine regulators was variable, but overall strong in the cancer cells and significantly lower or undetectable in PSCs. In cancer cells, hENT1 inhibition significantly downregulated gemcitabine uptake and cytotoxicity, whereas DCK knockdown reduced cytotoxicity. In conclusion, heterogeneity in gemcitabine processing among different pancreatic cancer cells and stellate cells results from the differential expression of molecular regulators which determines the effect of gemcitabine.

scholarly journals Pancreatic Cancer: The Role of Pancreatic Stellate Cells in Tumor Progression

Pancreatology ◽  
2011 ◽  
Vol 10 (6) ◽  
pp. 673-681 ◽  
Author(s):  
Siri Dunér ◽  
Jacob Lopatko Lindman ◽  
Daniel Ansari ◽  
Chinmay Gundewar ◽  
Roland Andersson
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Progression ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells

The TGFβ-SMAD3 pathway inhibits IL-1α induced cross talk between human pancreatic cancer cells and pancreatic stellate cells

Pancreatology ◽  
2015 ◽  
Vol 15 (3) ◽  
pp. S17
Author(s):  
Vegard Tjomsland ◽  
Dagny Sandnes ◽  
Ewa Pomianowska ◽  
Smiljana Torbica Cizmovic ◽  
Monica Aasrum ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cross Talk ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells
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