核梭杆菌
结直肠癌
癌变
小RNA
癌症研究
自噬
癌症
生物
医学
基因
内科学
遗传学
细菌
细胞凋亡
牙龈卟啉单胞菌
作者
Bin Tang,Xiaoxue Lu,Yanan Tong,Yuyang Feng,Yilan Mao,Guodong Dun,Jing Li,Qiao-Lin Xu,Jie Tang,Tao Zhang,Lei Deng,He Xiao,Yuanzhi Lan,Hua-xing Luo,Linghai Zeng,Yuanyuan Xiang,Qian Li,Da‐Wu Zeng,Xuhu Mao
出处
期刊:iScience
[Cell Press]
日期:2023-05-01
卷期号:26 (5): 106770-106770
被引量:2
标识
DOI:10.1016/j.isci.2023.106770
摘要
Persistent Fusobacterium nucleatum infection is associated with the development of human colorectal cancer (CRC) and promotes tumorigenicity, but the underlying mechanisms remain unclear. Here, we reported that F. nucleatum promoted the tumorigenicity of CRC, which was associated with F. nucleatum-induced microRNA-31 (miR-31) expression in CRC tissues and cells. F. nucleatum infection inhibited autophagic flux by miR-31 through inhibiting syntaxin-12 (STX12) and was associated with the increased intracellular survival of F. nucleatum. Overexpression of miR-31 in CRC cells promoted their tumorigenicity by targeting eukaryotic initiation factor 4F-binding protein 1/2 (eIF4EBP1/2), whereas miR-31 knockout mice were resistant to the formation of colorectal tumors. In conclusion, F. nucleatum, miR-31, and STX12 form a closed loop in the autophagy pathway, and continuous F. nucleatum-induced miR-31 expression promotes the tumorigenicity of CRC cells by targeting eIF4EBP1/2. These findings reveal miR-31 as a potential diagnostic biomarker and therapeutic target in CRC patients with F. nucleatum infection.
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