circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity

Botai Li, Lili Zhu, Chunlai Lu, Cun Wang, Hui Wang, Haojie Jin, Xuhui Ma, Zhuoan Cheng, Chengtao Yu, Siying Wang, Qiaozhu Zuo, Yangyang Zhou, Jun Wang, Chen Yang, Yuanyuan Lv, Liyan Jiang () and Wenxin Qin ()
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Botai Li: Shanghai Jiao Tong University School of Biomedical Engineering
Lili Zhu: Shanghai Jiao Tong University School of Biomedical Engineering
Chunlai Lu: Fudan University
Cun Wang: Shanghai Jiao Tong University School of Medicine
Hui Wang: Shanghai Jiao Tong University School of Medicine
Haojie Jin: Shanghai Jiao Tong University School of Medicine
Xuhui Ma: Shanghai Jiao Tong University School of Medicine
Zhuoan Cheng: Shanghai Jiao Tong University School of Biomedical Engineering
Chengtao Yu: Shanghai Jiao Tong University School of Biomedical Engineering
Siying Wang: Shanghai Jiao Tong University School of Medicine
Qiaozhu Zuo: Shanghai Jiao Tong University School of Medicine
Yangyang Zhou: Shanghai Jiao Tong University School of Medicine
Jun Wang: Shanghai Jiao Tong University School of Medicine
Chen Yang: Shanghai Jiao Tong University School of Medicine
Yuanyuan Lv: Shanghai Jiao Tong University School of Medicine
Liyan Jiang: Shanghai Jiao Tong University
Wenxin Qin: Shanghai Jiao Tong University School of Biomedical Engineering

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Circular RNAs (circRNA) are a class of covalently closed single-stranded RNAs that have been implicated in cancer progression. Here we identify circNDUFB2 to be downregulated in non-small cell lung cancer (NSCLC) tissues, and to negatively correlate with NSCLC malignant features. Elevated circNDUFB2 inhibits growth and metastasis of NSCLC cells. Mechanistically, circNDUFB2 functions as a scaffold to enhance the interaction between TRIM25 and IGF2BPs, a positive regulator of tumor progression and metastasis. This TRIM25/circNDUFB2/IGF2BPs ternary complex facilitates ubiquitination and degradation of IGF2BPs, with this effect enhanced by N6-methyladenosine (m6A) modification of circNDUFB2. Moreover, circNDUFB2 is also recognized by RIG-I to activate RIG-I-MAVS signaling cascades and recruit immune cells into the tumor microenvironment (TME). Our data thus provide evidences that circNDUFB2 participates in the degradation of IGF2BPs and activation of anti-tumor immunity during NSCLC progression via the modulation of both protein ubiquitination and degradation, as well as cellular immune responses.

Date: 2021
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DOI: 10.1038/s41467-020-20527-z

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