Contextual regulation of pancreatic cancer stem cell phenotype and radioresistance by pancreatic stellate cells
Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the...
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| Vydáno v: | Radiotherapy and oncology Ročník 111; číslo 2; s. 243 - 251 |
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| Hlavní autoři: | , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Ireland
Elsevier Ireland Ltd
01.05.2014
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| ISSN: | 0167-8140, 1879-0887, 1879-0887 |
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| Abstract | Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the role of these processes on the radioresponse and tumorigenicity of pancreatic cancer cells.
We used an in vitro sphere model and in vivo xenograft model to examine the role of PSC in EMT and CSC processes.
We demonstrated that PSC enhanced the CSC phenotype and radioresistance of pancreatic cancer cells. Furthermore, the expression of several EMT and CSC markers supported enhanced processes in our models and that translated into remarkable in vivo tumorigenicity. Multi-dose TGFβ neutralizing antibody inhibited the EMT and CSC processes, sensitized cells to radiation and reduced in vivo tumorigenicity. A proteomic screen identified multiple novel factors that were regulated by PSC in pancreatic cells.
These results are critical in highlighting the role of PSC in tumor progression and radioresistance by manipulating the EMT and CSC processes. TGFβ and the novel factors identified are important targets for better therapeutic outcome in response to PSC mediated mechanisms. |
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| AbstractList | Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the role of these processes on the radioresponse and tumorigenicity of pancreatic cancer cells.
We used an in vitro sphere model and in vivo xenograft model to examine the role of PSC in EMT and CSC processes.
We demonstrated that PSC enhanced the CSC phenotype and radioresistance of pancreatic cancer cells. Furthermore, the expression of several EMT and CSC markers supported enhanced processes in our models and that translated into remarkable in vivo tumorigenicity. Multi-dose TGFβ neutralizing antibody inhibited the EMT and CSC processes, sensitized cells to radiation and reduced in vivo tumorigenicity. A proteomic screen identified multiple novel factors that were regulated by PSC in pancreatic cells.
These results are critical in highlighting the role of PSC in tumor progression and radioresistance by manipulating the EMT and CSC processes. TGFβ and the novel factors identified are important targets for better therapeutic outcome in response to PSC mediated mechanisms. Abstract Background and purpose Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the role of these processes on the radioresponse and tumorigenicity of pancreatic cancer cells. Materials and methods We used an in vitro sphere model and in vivo xenograft model to examine the role of PSC in EMT and CSC processes. Results We demonstrated that PSC enhanced the CSC phenotype and radioresistance of pancreatic cancer cells. Furthermore, the expression of several EMT and CSC markers supported enhanced processes in our models and that translated into remarkable in vivo tumorigenicity. Multi-dose TGFβ neutralizing antibody inhibited the EMT and CSC processes, sensitized cells to radiation and reduced in vivo tumorigenicity. A proteomic screen identified multiple novel factors that were regulated by PSC in pancreatic cells. Conclusion These results are critical in highlighting the role of PSC in tumor progression and radioresistance by manipulating the EMT and CSC processes. TGFβ and the novel factors identified are important targets for better therapeutic outcome in response to PSC mediated mechanisms. Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the role of these processes on the radioresponse and tumorigenicity of pancreatic cancer cells.BACKGROUND AND PURPOSEProgression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression is epithelial mesenchymal transition (EMT), which shares many characteristics with the cancer stem cell (CSC) hypothesis. We investigated the role of these processes on the radioresponse and tumorigenicity of pancreatic cancer cells.We used an in vitro sphere model and in vivo xenograft model to examine the role of PSC in EMT and CSC processes.MATERIALS AND METHODSWe used an in vitro sphere model and in vivo xenograft model to examine the role of PSC in EMT and CSC processes.We demonstrated that PSC enhanced the CSC phenotype and radioresistance of pancreatic cancer cells. Furthermore, the expression of several EMT and CSC markers supported enhanced processes in our models and that translated into remarkable in vivo tumorigenicity. Multi-dose TGFβ neutralizing antibody inhibited the EMT and CSC processes, sensitized cells to radiation and reduced in vivo tumorigenicity. A proteomic screen identified multiple novel factors that were regulated by PSC in pancreatic cells.RESULTSWe demonstrated that PSC enhanced the CSC phenotype and radioresistance of pancreatic cancer cells. Furthermore, the expression of several EMT and CSC markers supported enhanced processes in our models and that translated into remarkable in vivo tumorigenicity. Multi-dose TGFβ neutralizing antibody inhibited the EMT and CSC processes, sensitized cells to radiation and reduced in vivo tumorigenicity. A proteomic screen identified multiple novel factors that were regulated by PSC in pancreatic cells.These results are critical in highlighting the role of PSC in tumor progression and radioresistance by manipulating the EMT and CSC processes. TGFβ and the novel factors identified are important targets for better therapeutic outcome in response to PSC mediated mechanisms.CONCLUSIONThese results are critical in highlighting the role of PSC in tumor progression and radioresistance by manipulating the EMT and CSC processes. TGFβ and the novel factors identified are important targets for better therapeutic outcome in response to PSC mediated mechanisms. |
| Author | Demiciorglu, Fevzi Gaspar-Carvalho, Maria Manuela Al-Assar, Osama Muschel, Ruth M. Brunner, Thomas B. McKenna, William Gillies Lunardi, Serena |
| Author_xml | – sequence: 1 givenname: Osama surname: Al-Assar fullname: Al-Assar, Osama – sequence: 2 givenname: Fevzi surname: Demiciorglu fullname: Demiciorglu, Fevzi – sequence: 3 givenname: Serena surname: Lunardi fullname: Lunardi, Serena – sequence: 4 givenname: Maria Manuela surname: Gaspar-Carvalho fullname: Gaspar-Carvalho, Maria Manuela – sequence: 5 givenname: William Gillies surname: McKenna fullname: McKenna, William Gillies – sequence: 6 givenname: Ruth M. surname: Muschel fullname: Muschel, Ruth M. – sequence: 7 givenname: Thomas B. surname: Brunner fullname: Brunner, Thomas B. email: thomas.brunner@uniklinik-freiburg.de |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24780634$$D View this record in MEDLINE/PubMed |
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| Keywords | Radioresistance Pancreatic stellate cells Epithelial mesenchymal transition Cancer stem-like cells Pancreatic cancer |
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| Snippet | Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC). Contributory to this progression... Abstract Background and purpose Progression of pancreatic ductal adenocarcinoma (PDAC) is promoted by desmoplasia induced by pancreatic stellate cells (PSC).... |
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| SubjectTerms | Adenocarcinoma - pathology Adenocarcinoma - radiotherapy Antibodies, Neutralizing - pharmacology Biomarkers, Tumor - analysis Cancer stem-like cells Carcinoma, Pancreatic Ductal - pathology Carcinoma, Pancreatic Ductal - radiotherapy Cell Survival - physiology Cell Survival - radiation effects Epithelial mesenchymal transition Epithelial-Mesenchymal Transition - physiology Fibroblasts - pathology Hematology, Oncology and Palliative Medicine Humans Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Neoplastic Stem Cells - radiation effects Pancreatic cancer Pancreatic Neoplasms - pathology Pancreatic Neoplasms - radiotherapy Pancreatic stellate cells Pancreatic Stellate Cells - physiology Phenotype Radiation Tolerance - physiology Radioresistance Transforming Growth Factor beta - metabolism Tumor Cells, Cultured |
| Title | Contextual regulation of pancreatic cancer stem cell phenotype and radioresistance by pancreatic stellate cells |
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