Cargando…

The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer

(1) Background: IL-17A accelerates pancreatic intraepithelial neoplasia (PanIN) progression. In this study, we examined whether IL-17A/IL-17RA promotes pancreatic ductal adenocarcinoma (PDAC) aggressiveness in terms of survival and cancer stem cell modulation. (2) Methods: In vitro, the wound-healin...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Jiahui, Betzler, Christopher, Lohneis, Philipp, Popp, Marie Christine, Qin, Jiwei, Kalinski, Thomas, Wartmann, Thomas, Bruns, Christiane J., Zhao, Yue, Popp, Felix C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139783/
https://www.ncbi.nlm.nih.gov/pubmed/32210079
http://dx.doi.org/10.3390/ijms21062215
_version_ 1783518846086283264
author Li, Jiahui
Betzler, Christopher
Lohneis, Philipp
Popp, Marie Christine
Qin, Jiwei
Kalinski, Thomas
Wartmann, Thomas
Bruns, Christiane J.
Zhao, Yue
Popp, Felix C.
author_facet Li, Jiahui
Betzler, Christopher
Lohneis, Philipp
Popp, Marie Christine
Qin, Jiwei
Kalinski, Thomas
Wartmann, Thomas
Bruns, Christiane J.
Zhao, Yue
Popp, Felix C.
author_sort Li, Jiahui
collection PubMed
description (1) Background: IL-17A accelerates pancreatic intraepithelial neoplasia (PanIN) progression. In this study, we examined whether IL-17A/IL-17RA promotes pancreatic ductal adenocarcinoma (PDAC) aggressiveness in terms of survival and cancer stem cell modulation. (2) Methods: In vitro, the wound-healing assay, the sphere formation assay, and flow cytometry were applied to assess cancer stem cell features. In vivo, pancreatic tumors were induced in C57BL/6 mice using electroporation with oncogenic plasmids (P53-/- R172H; KrasG12V). Anti-IL-17 antibodies were administered as immunotherapy. We analyzed IL-17A/IL-17RA related survival using publicly available transcriptomic data (n = 903). (3) Results: IL-17A/IL-17RA expression was not related to survival in PDAC patients. IL-17A neither induces stem cell markers nor increases sphere formation and cell motility in vitro. Blocking the IL-17A/IL-17RA axis in a murine pancreatic cancer model did not improve the survival of mice, but reduced the tumor burden slightly. (4) Conclusions: IL-17A does not promote stem cell expansion in PDAC cell lines. Blocking IL-17A/IL-17RA signaling does not interfere with pancreatic cancer development and progression and may not be considered as a promising monotherapy for PDAC.
format Online
Article
Text
id pubmed-7139783
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-71397832020-04-10 The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer Li, Jiahui Betzler, Christopher Lohneis, Philipp Popp, Marie Christine Qin, Jiwei Kalinski, Thomas Wartmann, Thomas Bruns, Christiane J. Zhao, Yue Popp, Felix C. Int J Mol Sci Communication (1) Background: IL-17A accelerates pancreatic intraepithelial neoplasia (PanIN) progression. In this study, we examined whether IL-17A/IL-17RA promotes pancreatic ductal adenocarcinoma (PDAC) aggressiveness in terms of survival and cancer stem cell modulation. (2) Methods: In vitro, the wound-healing assay, the sphere formation assay, and flow cytometry were applied to assess cancer stem cell features. In vivo, pancreatic tumors were induced in C57BL/6 mice using electroporation with oncogenic plasmids (P53-/- R172H; KrasG12V). Anti-IL-17 antibodies were administered as immunotherapy. We analyzed IL-17A/IL-17RA related survival using publicly available transcriptomic data (n = 903). (3) Results: IL-17A/IL-17RA expression was not related to survival in PDAC patients. IL-17A neither induces stem cell markers nor increases sphere formation and cell motility in vitro. Blocking the IL-17A/IL-17RA axis in a murine pancreatic cancer model did not improve the survival of mice, but reduced the tumor burden slightly. (4) Conclusions: IL-17A does not promote stem cell expansion in PDAC cell lines. Blocking IL-17A/IL-17RA signaling does not interfere with pancreatic cancer development and progression and may not be considered as a promising monotherapy for PDAC. MDPI 2020-03-23 /pmc/articles/PMC7139783/ /pubmed/32210079 http://dx.doi.org/10.3390/ijms21062215 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Communication
Li, Jiahui
Betzler, Christopher
Lohneis, Philipp
Popp, Marie Christine
Qin, Jiwei
Kalinski, Thomas
Wartmann, Thomas
Bruns, Christiane J.
Zhao, Yue
Popp, Felix C.
The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title_full The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title_fullStr The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title_full_unstemmed The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title_short The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer
title_sort il-17a/il-17ra axis is not related to overall survival and cancer stem cell modulation in pancreatic cancer
topic Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139783/
https://www.ncbi.nlm.nih.gov/pubmed/32210079
http://dx.doi.org/10.3390/ijms21062215
work_keys_str_mv AT lijiahui theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT betzlerchristopher theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT lohneisphilipp theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT poppmariechristine theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT qinjiwei theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT kalinskithomas theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT wartmannthomas theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT brunschristianej theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT zhaoyue theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT poppfelixc theil17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT lijiahui il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT betzlerchristopher il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT lohneisphilipp il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT poppmariechristine il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT qinjiwei il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT kalinskithomas il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT wartmannthomas il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT brunschristianej il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT zhaoyue il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer
AT poppfelixc il17ail17raaxisisnotrelatedtooverallsurvivalandcancerstemcellmodulationinpancreaticcancer