circCsnk1g3- and circAnkib1-regulated interferon responses in sarcoma promote tumorigenesis by shaping the immune microenvironment

Roberta Piras, Emily Y. Ko, Connor Barrett, Marco Simone, Xianzhi Lin, Marina T. Broz, Fernando H. G. Tessaro, Mireia Castillo-Martin, Carlos Cordon-Cardo, Helen S. Goodridge, Dolores Vizio, Mona Batish, Kate Lawrenson, Y. Grace Chen, Keith Syson Chan and Jlenia Guarnerio ()
Additional contact information
Roberta Piras: Cedars-Sinai Medical Center
Emily Y. Ko: Cedars-Sinai Medical Center
Connor Barrett: University of Delaware
Marco Simone: Cedars-Sinai Medical Center
Xianzhi Lin: Cedars-Sinai Medical Center
Marina T. Broz: Cedars-Sinai Medical Center
Fernando H. G. Tessaro: Cedars-Sinai Medical Center
Mireia Castillo-Martin: The Mount Sinai Medical Center
Carlos Cordon-Cardo: The Mount Sinai Medical Center
Helen S. Goodridge: Cedars-Sinai Medical Center
Dolores Vizio: Cedars-Sinai Medical Center
Mona Batish: University of Delaware
Kate Lawrenson: Cedars-Sinai Medical Center
Y. Grace Chen: Yale University School of Medicine
Keith Syson Chan: Cedars-Sinai Medical Center
Jlenia Guarnerio: Cedars-Sinai Medical Center

Nature Communications, 2022, vol. 13, issue 1, 1-14

Abstract: Abstract Exonic circular RNAs (circRNAs) produce predominantly non-coding RNA species that have been recently profiled in many tumors. However, their functional contribution to cancer progression is still poorly understood. Here, we identify the circRNAs expressed in soft tissue sarcoma cells and explore how the circRNAs regulate sarcoma growth in vivo. We show that circCsnk1g3 and circAnkib1 promote tumor growth by shaping a pro-tumorigenic microenvironment, possibly due to their capabilities to regulate tumor-promoting elements extrinsic to the tumor cells. Accordingly, circCsnk1g3 and circAnkib1 can control the expression of interferon-related genes and pro-inflammatory factors in the sarcoma cells, thus directing immune cell recruitment into the tumor mass, and hence their activation. Mechanistically, circRNAs may repress pro-inflammatory elements by buffering activation of the pathways mediated by RIG-I, the cytosolic viral RNA sensor. The current findings suggest that the targeting of specific circRNAs could augment the efficacy of tumor and immune response to mainstay therapies.

Date: 2022
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DOI: 10.1038/s41467-022-34872-8

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