Periostin, secreted from stromal cells, has biphasic effect on cell migration and correlates with the epithelial to mesenchymal transition of human pancreatic cancer cells

2008 ◽  
Vol 122 (12) ◽  
pp. 2707-2718 ◽  
Author(s):  
Atsushi Kanno ◽  
Kennichi Satoh ◽  
Atsushi Masamune ◽  
Morihisa Hirota ◽  
Kenji Kimura ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Human Pancreatic Cancer ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells ◽  
Biphasic Effect

scholarly journals RAGE Up-Regulation Differently Affects Cell Proliferation and Migration in Pancreatic Cancer Cells

2020 ◽  
Vol 21 (20) ◽  
pp. 7723
Author(s):  
Priyanka Swami ◽  
Swetha Thiyagarajan ◽  
Arianna Vidger ◽  
Venkata S. K. Indurthi ◽  
Stefan W. Vetter ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

The receptor for advanced glycation end products (RAGE) contributes to many cellular aspects of pancreatic cancer including cell proliferation, migration, and survival. Studies have shown that RAGE activation by its ligands promotes pancreatic tumor growth by stimulating both cell proliferation and migration. In this study, we investigated the effect of RAGE up-regulation on the proliferation and migration of the human pancreatic cancer Panc-1 cell-line. We show that moderate overexpression of RAGE in Panc-1 cells results in increased cell proliferation, but decreased cell migration. The observed cellular changes were confirmed to be RAGE-specific and reversible by using RAGE-specific siRNAs and the small molecule RAGE inhibitor FPS-ZM1. At the molecular level, we show that RAGE up-regulation was associated with decreased activity of FAK, Akt, Erk1/2, and NF-κB signaling pathways and greatly reduced levels of α2 and β1 integrin expression, which is in agreement with the observed decreases in cell migration. We also demonstrate that RAGE up-regulation changes the expression of key molecular markers of epithelial-to-mesenchymal transition (EMT). Our results suggest that in the absence of stimulation by external ligands, RAGE up-regulation can differently modulate cell proliferation and migration in pancreatic cancer cells and regulates partly EMT.

Effect of zeb1 and zeb2 on pancreatic fibrobast-induced epithelial-to-mesenchymal transition (EMT) in pancreatic cancer.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e21035-e21035
Author(s):  
Laura Visa ◽  
Esther Samper ◽  
Mariana Rickmann ◽  
Antonio Postigo ◽  
Esther Sanchez-Tillo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Smooth Muscle Actin ◽  
Human Pancreatic Cancer ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Epithelial Tumor ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells ◽  
E Cadherin

e21035 Background: EMT renders neoplastic cancer cells the ability to migrate and to invade distant organs. The hallmark of EMT is the loss of E-cadherin, which is a prerequisite for epithelial tumor cell invasion. In pancreatic cancer, loss of tumor E-cadherin is an independent predictor of poor outcome. Aims: To analyze the effect of pancreatic fibroblasts (PF) on inducing EMT in pancreatic cancer cells and to identify the transcription factors (Snail, Slug, ZEB1, ZEB2) that mediate EMT process. Methods: Human PFs were isolated from human pancreatic specimens obtained from chronic pancreatitis and from unaffected margins of pancreatic adenocarcinoma and serous cistoadenoma. PF were cultured until complete cellular activation, as assessed by expression of α-smooth muscle actin, vimentin and fibronectin. Human pancreatic cancer cells Panc-1 were exposed to PF conditioned medium (PF-CM) and EMT analyzed by cell morphology, migration, and E-cadherin expression (quantitative RT-PCR and immunoblot). Gene expression of Snail, Slug, ZEB1, and ZEB2 was analyzed by quantitative RT-PCR, and their activity modulated by siRNA Results: Conditioned media from all types of activated PFs induced EMT changes in Panc-1 cells, as shown by 1) morphological transition from cobblestone shaped to fibroblast-like cells, 2) stimulation of cell migration, and 3) E-cadherin down–regulation; mRNA expression of Snail transiently increased at 30 min after exposure to PF returning to basal levels afterwards; mRNA levels of ZEB1 were not up-regulated upon exposure to PF-CM. However, ZEB1 protein greatly accumulated after 48h incubation with PF-CM, suggesting that PF prevent ZEB1 degradation in Panc-1 cells. Combined RNA downregulation of ZEB1 and ZEB2, but not of Snail and/or Slug, suppressed E-cadherin repression induced by PF. Conclusions: Activated PFs promote the invasive phenotype of pancreatic cancer cells through ZEB1 and ZEB2 activation.

scholarly journals Truncated O‐glycans promote epithelial‐to‐mesenchymal transition and stemness properties of pancreatic cancer cells

2019 ◽  
Vol 23 (10) ◽  
pp. 6885-6896 ◽  
Author(s):  
Divya Thomas ◽  
Satish Sagar ◽  
Thomas Caffrey ◽  
Paul M. Grandgenett ◽  
Prakash Radhakrishnan
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document