ADAR1 deficiency in pancreatic cancer cells potentiates cDC1 activation and promotes sensitization to immunotherapy.

Authors

Botai Li, Xiaoshuang Wang, Bowen Xie, Xuan Zhong, Peng Wei, Xinyi Lou, Ting Zhang, Chen Dong

Published in

Cancer immunology research. Jun 17, 2026. Epub Jun 17, 2026.

Abstract

Pancreatic cancer responds poorly to immunotherapy, primarily due to poor activation of CD8+ T cells and their limited infiltration into the tumor tissue. Strategies to enhance CD8+ T-cell priming and function are therefore critical for improving immunotherapeutic efficacy in pancreatic cancer. The RNA-editing enzyme adenosine deaminase acting on RNA 1 (ADAR1) plays a pivotal role in maintaining immune homeostasis. In this study, we found that ADAR1 expression positively correlates with pancreatic cancer progression. Depletion of ADAR1 in tumor cells resulted in excessive production of IFNβ, which increased the abundance and activation of conventional type 1 dendritic cells (cDC1s). This alteration enhanced CD8+ T-cell recruitment and activation, ultimately sensitizing pancreatic cancer to immunotherapy. Collectively, our findings support ADAR1 inhibition combined with immunotherapy as a promising therapeutic strategy for pancreatic cancer.

PMID:
42308348
Bibliographic data and abstract were imported from PubMed on 18 Jun 2026.

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