scholarly journals miR-367 promotes epithelial-to-mesenchymal transition and invasion of pancreatic ductal adenocarcinoma cells by targeting the Smad7-TGF-β signalling pathway

2015 ◽  
Vol 112 (8) ◽  
pp. 1367-1375 ◽  
Author(s):  
Z Zhu ◽  
Y Xu ◽  
J Zhao ◽  
Q Liu ◽  
W Feng ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Signalling Pathway ◽  
Ductal Adenocarcinoma ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells

scholarly journals BRM270 Inhibits the Proliferation of CD44 Positive Pancreatic Ductal Adenocarcinoma Cells via Downregulation of Sonic Hedgehog Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Do Luong Huynh ◽  
Hyebin Koh ◽  
Nisansala Chandimali ◽  
Jiao Jiao Zhang ◽  
Nameun Kim ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Ductal Adenocarcinoma ◽  
Cell Phenotype ◽  
Sonic Hedgehog Signaling ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells ◽  
Adenocarcinoma Cells

Pancreatic cancer has a poor survival rate as compared to other types of cancer. Surface marker CD44 plays important role in epithelial-mesenchymal transition and cancer stem cell phenotype. Therefore, targeting CD44 positive pancreatic cancer cells might enhance therapies effectiveness. Our previous studies indicated the antitumorigenesis effect of BRM270 in osteosarcoma, lung cancer, and glioblastoma; however there is no evidence on BRM270 impacts on pancreatic cancer growth. In this study, we investigated the effect of BRM270 on the isolated CD44 positive pancreatic ductal adenocarcinoma cells (CD44+PDAC). Results showed that CD44 positive cells undergo apoptosis induced by BRM270. Moreover, BRM270 also inhibits stemness and metastasis traits in CD44+PDAC via Sonic hedgehog signaling pathway and SALL4 expression.In vivostudy indicated that tumor growth derived from CD44+PDAC was suppressed as daily uptake by BRM270 5 mg/kg. These data suggest the alternative approach in antipancreatic tumorigenesis via herbal plants extract and selectively targeting CD44+PDAC cells in tumor.

Epithelial to mesenchymal transition and its reversal in metastasis of pancreatic ductal adenocarcinoma

2010 ◽  
Vol 211 (3) ◽  
pp. S12
Author(s):  
Wolf Arif Mardin ◽  
Soeren Torge Mees ◽  
Christina Haane ◽  
Sabrina Irmscher ◽  
Joerg Haier ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Ductal Adenocarcinoma ◽  
Mesenchymal Transition

scholarly journals Prognostic Role of High-Grade Tumor Budding in Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-Analysis with a Focus on Epithelial to Mesenchymal Transition

Cancers ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 113 ◽  
Author(s):  
Rita Lawlor ◽  
Nicola Veronese ◽  
Alessia Nottegar ◽  
Giuseppe Malleo ◽  
Lee Smith ◽  
...  
Keyword(s):  
Systematic Review ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Meta Analysis ◽  
Tumor Budding ◽  
Ductal Adenocarcinoma ◽  
High Grade ◽  
Prognostic Role ◽  
Mesenchymal Transition

This study aims at clarifying the prognostic role of high-grade tumor budding (TB) in pancreatic ductal adenocarcinoma (PDAC) with the first systematic review and meta-analysis on this topic. Furthermore, we analyzed with a systematic review the relationship between TB and a recently suggested TB-associated mechanism: the epithelial to mesenchymal transition (EMT). Analyzing a total of 613 patients, 251 of them (40.9%) with high grade-TB, we found an increased risk of all-cause mortality (RR, 1.46; 95% CI, 1.13–1.88, p = 0.004; HR, 2.65; 95% CI, 1.79–3.91; p < 0.0001) and of recurrence (RR, 1.61; 95% CI, 1.05–2.47, p = 0.03) for PDAC patients with high-grade TB. Moreover, we found that EMT is a central process in determining the presence of TB in PDAC. Thanks to this meta-analysis, we demonstrate the potential clinical significance of high-grade TB for prognostic stratification of PDAC. TB also shows a clear association with the process of EMT. Based on the results of the present study, TB should be conveyed in pathology reports and taken into account by future oncologic staging systems.

scholarly journals Epithelial-to-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma and Pancreatic Tumor Cell Lines: The Role of Neutrophils and Neutrophil-Derived Elastase

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Thomas Große-Steffen ◽  
Thomas Giese ◽  
Nathalia Giese ◽  
Thomas Longerich ◽  
Peter Schirmacher ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Pancreatic Tumor ◽  
Polymorphonuclear Neutrophils ◽  
Nuclear Accumulation ◽  
Ductal Adenocarcinoma ◽  
Mesenchymal Transition ◽  
E Cadherin

Pancreatic ductal adenocarcinoma (PDAC) is frequently associated with fibrosis and a prominent inflammatory infiltrate in the desmoplastic stroma. Moreover, in PDAC, an epithelial-to-mesenchymal transition (EMT) is observed. To explore a possible connection between the infiltrating cells, particularly the polymorphonuclear neutrophils (PMN) and the tumor cell transition, biopsies of patients with PDAC (n=115) were analysed with regard to PMN infiltration and nuclear expression ofβ-catenin and of ZEB1, well-established indicators of EMT. In biopsies with a dense PMN infiltrate, a nuclear accumulation ofβ-catenin and of ZEB1 was observed. To address the question whether PMN could induce EMT, they were isolated from healthy donors and were cocultivated with pancreatic tumor cells grown as monolayers. Rapid dyshesion of the tumor cells was seen, most likely due to an elastase-mediated degradation of E-cadherin. In parallel, the transcription factor TWIST was upregulated,β-catenin translocated into the nucleus, ZEB1 appeared in the nucleus, and keratins were downregulated. EMT was also induced when the tumor cells were grown under conditions preventing attachment to the culture plates. Here, also in the absence of elastase, E-cadherin was downmodulated. PMN as well as prevention of adhesion induced EMT also in liver cancer cell line. In conclusion, PMN via elastase induce EMTin vitro, most likely due to the loss of cell-to-cell contact. Because in pancreatic cancers the transition to a mesenchymal phenotype coincides with the PMN infiltrate, a contribution of the inflammatory response to the induction of EMT and—by implication—to tumor progression is possible.

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