IL-17B/RB Activation in Pancreatic Stellate Cells Promotes Pancreatic Cancer 
Metabolism and Growth

Li, J.; Wu, X.; Schiffmann, L.; MacVicar, T.; Zhou, C.; Wang, Z.; Li, D.; Camacho, O. V.; Heuchel, R.; Odenthal, M.; Hillmer, A.; Quaas, A.; Zhao, Y.; Bruns, C. J.; Popp, F. C.

doi:10.3390/cancers13215338

アイテム詳細

登録内容を編集ファイル形式で保存

一時保存へ追加

タグ情報を表示リリース履歴を表示詳細要約

公開

学術論文

IL-17B/RB Activation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Metabolism and Growth

MPS-Authors

/persons/resource/persons278027

MacVicar, T.
Department Langer - Mitochondrial Proteostasis, Max Planck Institute for Biology of Ageing, Max Planck Society;

External Resource

https://pubmed.ncbi.nlm.nih.gov/34771503/
(全文テキスト（全般）)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

フルテキスト (公開)

公開されているフルテキストはありません

付随資料 (公開)

There is no public supplementary material available

引用

Li, J., Wu, X., Schiffmann, L., MacVicar, T., Zhou, C., Wang, Z., Li, D., Camacho, O. V., Heuchel, R., Odenthal, M., Hillmer, A., Quaas, A., Zhao, Y., Bruns, C. J., & Popp, F. C. (2021). IL-17B/RB Activation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Metabolism and Growth. Cancers (Basel), 13(21). doi:10.3390/cancers13215338.

引用: https://hdl.handle.net/21.11116/0000-000A-FA89-2

要旨

In pancreatic ductal adenocarcinoma (PDAC), the tumor stroma constitutes most of the cell mass and contributes to therapy resistance and progression. Here we show a hitherto unknown metabolic cooperation between pancreatic stellate cells (PSCs) and tumor cells through Interleukin 17B/Interleukin 17B receptor (IL-17B/IL-17RB) signaling. Tumor-derived IL-17B carrying extracellular vesicles (EVs) activated stromal PSCs and induced the expression of IL-17RB. PSCs increased oxidative phosphorylation while reducing mitochondrial turnover. PSCs activated tumor cells in a feedback loop. Tumor cells subsequently increased oxidative phosphorylation and decreased glycolysis partially via IL-6. In vivo, IL-17RB overexpression in PSCs accelerated tumor growth in a co-injection xenograft mouse model. Our results demonstrate a tumor-to-stroma feedback loop increasing tumor metabolism to accelerate tumor growth under optimal nutritional conditions.