Loss of interleukin-13-receptor-alpha-1 induces apoptosis and promotes EMT in pancreatic cancer
peer-reviewed
Erstveröffentlichung
2022-03-26Authors
Shi, Jingwei
Shen, Xiao
Kang, Qi
Yang, Xing
Denzinger, Maximilian
Editor
Azmi, Asfar S.
Wissenschaftlicher Artikel
Published in
International Journal of Molecular Sciences ; 23 (2022), 7. - Art.-Nr. 3659. - eISSN 1422-0067
Link to original publication
https://dx.doi.org/10.3390/ijms23073659Institutions
UKU. Klinik für Allgemein- und ViszeralchirurgieDocument version
published version (publisher's PDF)Abstract
In search of new therapies for pancreatic cancer, cytokine pathways have attracted increasing interest in recent years. Cytokines play a vital role in the crosstalk between tumour cells and the tumour microenvironment. The related inflammatory cytokines IL-4 and IL-13 can regularly be detected at increased levels in the microenvironment of pancreatic cancer. They share a receptor heterodimer consisting of IL-4Rα and IL-13Rα1. While IL-4Rα induces a more oncogenic phenotype, the role of IL-13Rα1 was yet to be determined. ShRNA-based knockdown of IL-13Rα1 was performed in Capan-1 and MIA PaCa-2. We assessed cell growth and migratory capacities under the influence of IL-13Rα1. Pathway alterations were detected by immunoblot analysis. We now have demonstrated that the loss of IL-13Rα1 induces apoptosis in pancreatic cancer cells. This was associated with an epithelial-to-mesenchymal transition. Loss of IL-13Rα1 also abolished the effects of exogenous IL-4 and IL-13 stimulation. Interestingly, in wild type cells, cytokine stimulation caused a similar increase in migratory capacities as after IL-13Rα1 knockdown. Overall, our results indicate the vital role of IL-13Rα1 in the progression of pancreatic cancer. The differential expression of IL-4Rα and IL-13Rα1 has to be taken into account when considering a cytokine-targeted therapy in pancreatic cancer.
Is supplemented by
https://www.mdpi.com/article/10.3390/ijms23073659/s1Subject headings
[GND]: Bauchspeicheldrüsenkrebs | Interleukin 4 | Interleukin 13 | Cytokine | Immunoblot[MeSH]: Pancreatic neoplasms; Therapy | Cytokines | Interleukin-4 | Interleukin-13 | Receptors, Interleukin
[Free subject headings]: interleukin-13-receptor-alpha-1 | EMT | pancreatic cancer progression
[DDC subject group]: DDC 570 / Life sciences | DDC 610 / Medicine & health
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Show full item recordDOI & citation
Please use this identifier to cite or link to this item: http://dx.doi.org/10.18725/OPARU-47801
Shi, Jingwei et al. (2023): Loss of interleukin-13-receptor-alpha-1 induces apoptosis and promotes EMT in pancreatic cancer. Open Access Repositorium der Universität Ulm und Technischen Hochschule Ulm. http://dx.doi.org/10.18725/OPARU-47801
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