Yiqi Sun
*
Chao Zhong
*The final, formatted version of the article will be published soon.
REVIEW article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 15 - 2024 |
doi: 10.3389/fimmu.2024.1512353
This article is part of the Research Topic RNA Methylation and Demethylation in Tumorigenesis and as Therapeutic Targets View all articles
m5C methylation modification may be an accomplice in colorectal cancer escaping from anti-tumor effects of innate immunity-type I/III interferon
Provisionally accepted- Sichuan Provincial People's Hospital，University of Electronic Science and Technology of China， Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital., Chengdu, Sichuan Province, China
Colorectal cancer (CRC) is one of the most prevalent malignant tumors in the world, and its occurrence and development are closely related to the complex immune regulatory mechanisms. As the first barrier of the body's defense, innate immunity plays a key role in tumor immune surveillance and anti-tumor response, in which type I/III interferon (IFN) is an important mediator with significant antiviral and anti-tumor functions. 5-methylcytosine (m5C) modification of RNA is a key epigenetic regulation that promotes the expression of CRC oncogenes and immune-related genes. It can enhance the proliferation, migration, and invasion of tumor cells by affecting mRNA stability, translation efficiency, and nuclear export. In addition, m5C modification modulates the activity of innate immune signaling pathways and inhibits interferon production and function, further helping tumor cells evade immune surveillance. However, there are insufficient elucidations on the interaction between m5C modification and innate immunity in CRC. In this study, the mechanism of interferon I/III in colorectal cancer was systematically reviewed and explored. This work focused on how m5C modification promotes tumor immune escape by affecting the interferon signaling pathway, thereby providing new diagnostic markers and therapeutic targets for clinical use, and enhancing the immunotherapy efficacy.
Keywords: m5C methylation, colorectal cancer, type I/III interferon, tumor immune escape, Innate immune signaling pathways
Received: 16 Oct 2024; Accepted: 19 Dec 2024.
Copyright: © 2024 Sun, Liu, Jiang and Zhong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yiqi Sun, Sichuan Provincial People's Hospital，University of Electronic Science and Technology of China， Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital., Chengdu, Sichuan Province, China
Yunfei Liu, Sichuan Provincial People's Hospital，University of Electronic Science and Technology of China， Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital., Chengdu, Sichuan Province, China
Lu Jiang, Sichuan Provincial People's Hospital，University of Electronic Science and Technology of China， Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital., Chengdu, Sichuan Province, China
Chao Zhong, Sichuan Provincial People's Hospital，University of Electronic Science and Technology of China， Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital., Chengdu, Sichuan Province, China
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