Journal of Zhejiang University SCIENCE  B

Accepted manuscript available online (unedited version)


Mitochondrial double-stranded RNA escape checkpoints in cancer: immune decoding, immunoediting and therapeutic rewiring


Author(s):  Sajid ALI1, Wajid ZAMAN2

Affiliation(s):  1Department of Horticulture and Life Science, Yeungnam University, Gyeongsan 38541, Republic of Korea; more

Corresponding email(s):  wajidzaman@yu.ac.kr

Key Words:  Mitochondrial double-stranded RNA, Viral mimicry, RIG-I-like receptors, Innate immunity, Cancer immunotherapy


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.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

Open peer comments: Debate/Discuss/Question/Opinion

<1>

Please provide your name, email address and a comment





Full Text:  <12>

CLC number: 

On-line Access: 2026-10-23

Received: 2026-08-10

Revision Accepted: 2026-10-13

Crosschecked: 0000-00-00

Cited: 0

Clicked: 19

Citations:  Bibtex RefMan EndNote GB/T7714

Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou 310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn
Copyright © 2000 - 2026 Journal of Zhejiang University-SCIENCE