Affiliation(s): 1Department of Horticulture and Life Science, Yeungnam University, Gyeongsan 38541, Republic of Korea;
moreAffiliation(s): 1Department of Horticulture and Life Science, Yeungnam University, Gyeongsan 38541, Republic of Korea; 2Department of Life Sciences, Yeungnam University, Gyeongsan 38541, Republic of Korea;
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Sajid ALI1, Wajid ZAMAN2. Mitochondrial double-stranded RNA escape checkpoints in cancer: immune decoding, immunoediting and therapeutic rewiring[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2600620
@article{title="Mitochondrial double-stranded RNA escape checkpoints in cancer: immune decoding, immunoediting and therapeutic rewiring", author="Sajid ALI1, Wajid ZAMAN2", journal="Journal of Zhejiang University Science B", year="in press", publisher="Zhejiang University Press & Springer", doi="https://doi.org/10.1631/jzus.B2600620" }
%0 Journal Article %T Mitochondrial double-stranded RNA escape checkpoints in cancer: immune decoding, immunoediting and therapeutic rewiring %A Sajid ALI1 %A Wajid ZAMAN2 %J Journal of Zhejiang University SCIENCE B %P %@ 1673-1581 %D in press %I Zhejiang University Press & Springer doi="https://doi.org/10.1631/jzus.B2600620"
TY - JOUR T1 - Mitochondrial double-stranded RNA escape checkpoints in cancer: immune decoding, immunoediting and therapeutic rewiring A1 - Sajid ALI1 A1 - Wajid ZAMAN2 J0 - Journal of Zhejiang University Science B SP - EP - %@ 1673-1581 Y1 - in press PB - Zhejiang University Press & Springer ER - doi="https://doi.org/10.1631/jzus.B2600620"
Abstract: Mitochondrial double-stranded RNA (mt-dsRNA) can act as an immune signal; however, its effects in cancer depend on where it is generated, buffered, released, and sensed. Herein, we synthesize evidence for four linked checkpoints: duplex formation and modification, intramitochondrial degradation, membrane escape, and receptor-specific decoding. It is found that human-cell and trafficking studies demonstrate that mitochondrial RNA surveillance constrains mt-dsRNA and that a fraction can reach the cytosol. Cancer studies report distinct outcomes: altered mitochondrial RNA turnover can affect acute myeloid leukemia cell state, tumor-derived mt-dsRNA can remodel B-cell leukemia stroma, and pancreatic cancer-associated sensing supports growth. However, these findings do not establish a pan-cancer dependency; we propose that source, compartment, sensor, recipient cell, and signal duration must be resolved before therapeutic direction is assigned. In addition, we outline assays and biomarkers that distinguish an acute antitumor response from chronic inflammation, tumor-supportive signaling, or normal-tissue toxicity. This framework also guides biomarker selection and treatment scheduling, while the clinical benefit remains to be validated.
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