Secreted growth factors from stromal fibroblasts of the human lung and pancreatic carcinomas

Kopantzev, E. P.; Мелехина, О. В.; Kopantseva, M. R.; Мочальникова, В В; Виноградова, Т. В.; Егоров, В. Н.; Зборовская, И. Б.; Fedorov, A. V.

doi:10.1134/s0012496609060283

Cited by 3 publications

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“…We earlier demonstrated that the stromal cells of pancreatic tumors produced a variety of growth factors that had cell transforming and cell growth stimulat ing activities [12]. In particular, the protein factors TGF β, HGF, and IGF1 were identified in a condi tioned media of stromal cells; these proteins were capable of inducing in certain cells the synthesis of proteins SNAIL, TWIST, ZEB1, and ZEB2, which control epithelial mesenchymal transition in both normal and tumor epithelial cells.…”

Section: Expression Of the Zeb2 Gene In Pancreatic Stromal Cells In Pmentioning

confidence: 99%

Expression of the ZEB2 gene in pancreatic stromal cells in pancreatic ductal adenocarcinoma, pancreatitis, and normal state

et al. 2013

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Section: Expression Of the Zeb2 Gene In Pancreatic Stromal Cells In Pmentioning

confidence: 99%

Expression of the ZEB2 gene in pancreatic stromal cells in pancreatic ductal adenocarcinoma, pancreatitis, and normal state

et al. 2013

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The correlation of hematopoietic stem cells with cancer stem cells through the regulation of stromal cells in tumor microenvironment

Lin

2013

Medical Hypotheses

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Met Receptor Tyrosine Kinase Signaling Induces Secretion of the Angiogenic Chemokine Interleukin-8/CXCL8 in Pancreatic Cancer

et al. 2012

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At diagnosis, the majority of pancreatic cancer patients present with advanced disease when curative resection is no longer feasible and current therapeutic treatments are largely ineffective. An improved understanding of molecular targets for effective intervention of pancreatic cancer is thus urgent. The Met receptor tyrosine kinase is one candidate implicated in pancreatic cancer. Notably, Met is over expressed in up to 80% of invasive pancreatic cancers but not in normal ductal cells correlating with poor overall patient survival and increased recurrence rates following surgical resection. However the functional role of Met signaling in pancreatic cancer remains poorly understood. Here we used RNA interference to directly examine the pathobiological importance of increased Met signaling for pancreatic cancer. We show that Met knockdown in pancreatic tumor cells results in decreased cell survival, cell invasion, and migration on collagen I in vitro. Using an orthotopic model for pancreatic cancer, we provide in vivo evidence that Met knockdown reduced tumor burden correlating with decreased cell survival and tumor angiogenesis, with minimal effect on cell growth. Notably, we report that Met signaling regulates the secretion of the pro-angiogenic chemokine interleukin-8/CXCL8. Our data showing that the interleukin-8 receptors CXCR1 and CXCR2 are not expressed on pancreatic tumor cells, suggests a paracrine mechanism by which Met signaling regulates interleukin-8 secretion to remodel the tumor microenvironment, a novel finding that could have important clinical implications for improving the effectiveness of treatments for pancreatic cancer.

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Secreted growth factors from stromal fibroblasts of the human lung and pancreatic carcinomas

Cited by 3 publications

References 7 publications

Expression of the ZEB2 gene in pancreatic stromal cells in pancreatic ductal adenocarcinoma, pancreatitis, and normal state

Expression of the ZEB2 gene in pancreatic stromal cells in pancreatic ductal adenocarcinoma, pancreatitis, and normal state

The correlation of hematopoietic stem cells with cancer stem cells through the regulation of stromal cells in tumor microenvironment

Met Receptor Tyrosine Kinase Signaling Induces Secretion of the Angiogenic Chemokine Interleukin-8/CXCL8 in Pancreatic Cancer

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