Chronic type II interferon promotes tumor growth through mitochondrial RNA–induced type I interferon and prostaglandin synthesis

Interferons (IFNs) are proinflammatory cytokines that promote immune cell engagement to eliminate malignant cells. Paradoxically, chronic interferon signaling can also activate anti-inflammatory mechanisms that allow cancer cells to evade the immune system. In this study, we sought to determine the cellular mechanisms underlying this switch from antitumorigenic to protumorigenic interferon activity. We show that chronic type II interferon (IFN-II) exposure distinctively induced tumor growth by activating a type I interferon (IFN-I) response mediated by release of double-stranded mitochondrial RNA (ds-mtRNA) into the cytoplasm. This IFN-I signal synergized with IFN-II to enhance tumor growth by increasing immunosuppressive prostaglandin E 2 (PGE 2 ) synthesis through increased cyclooxygenase 2 expression. Elimination of PGE 2 synthesis in immunotherapy-resistant melanoma cells restored their responsiveness to anti-PD1 treatment, indicating that this covert mtRNA-IFN-prostaglandin pathway could be a therapeutic target to combat immunotherapy resistance.

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Publication Details

Journal
Science
Published
2026-09-10
DOI
https://doi.org/10.1126/science.aec0002
Primary Topic
interferon and immune responses
Type
article
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article

Chronic type II interferon promotes tumor growth through mitochondrial RNA–induced type I interferon and prostaglandin synthesis

Gladys R. Rojas, Kathryn Lande, Kailash Chandra Mangalhara, Mack B. Reynolds et al.
Science
interferon and immune responses
article

Chronic type II interferon promotes tumor growth through mitochondrial RNA–induced type I interferon and prostaglandin synthesis

Gladys R. Rojas, Kathryn Lande, Kailash Chandra Mangalhara, Mack B. Reynolds, Karl A. Wessendorf-Rodriguez, Pau B. Esparza‐Moltó, Ziyan Xu, Christian M. Metallo, Neva Olliffe, Alexandra G Moyzis, Sagnika Ghosh, Siva Karthik Varanasi, Matthew P. Donnelly, Victoria Tripple, Gerald S. Shadel, Susan M. Kaech, Melissa Johnson, Diana C. Hargreaves, Michael A. LaPorta, Susan M. Kaech, Kym J. Grae, Rebecca R Chinn
article en

Abstract

Interferons (IFNs) are proinflammatory cytokines that promote immune cell engagement to eliminate malignant cells. Paradoxically, chronic interferon signaling can also activate anti-inflammatory mechanisms that allow cancer cells to evade the immune system. In this study, we sought to determine the cellular mechanisms underlying this switch from antitumorigenic to protumorigenic interferon activity. We show that chronic type II interferon (IFN-II) exposure distinctively induced tumor growth by activating a type I interferon (IFN-I) response mediated by release of double-stranded mitochondrial RNA (ds-mtRNA) into the cytoplasm. This IFN-I signal synergized with IFN-II to enhance tumor growth by increasing immunosuppressive prostaglandin E 2 (PGE 2 ) synthesis through increased cyclooxygenase 2 expression. Elimination of PGE 2 synthesis in immunotherapy-resistant melanoma cells restored their responsiveness to anti-PD1 treatment, indicating that this covert mtRNA-IFN-prostaglandin pathway could be a therapeutic target to combat immunotherapy resistance.

ScienceVol. 393(6816)
Salk Institute for Biological Studies (US), Sanford Burnham Prebys Medical Discovery Institute (US), Discovery Institute (US), University of California San Diego (US), University of California San Diego Medical Center (US), La Jolla Bioengineering Institute (US)
Good health and well-being
Openalex Percentile: Top 17%
interferon and immune responses
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