An anti-invasion endogenous tRNA-derived small RNA (3'-tRFAlaAGC) alleviates endometriosis by suppressing MCCC1 mediated EMT

Hengmei Shi, Senhui Zhang, Huyang Hou, Tong Li, Danni He, Deshuo Jiang, Xin Cheng, Le Ma, Xuan Lin, Yangkaiyuan Liu, Y. Liu, Zheng Ding, Hongjie Ruan, Ziyi Fu, Xiaoyan Shi
Cellular signalling · 2026 · pp. 112990 · doi:10.1016/j.cellsig.2026.112990 · PMID:42982359 · W7225225676
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Abstract

Endometriosis is an invasive gynecological disorder, characterized by occult ectopic endometrial growth. Nascent endogenous tRNA-derived fragments occur across various disease, yet its pathology mechanistic pathways in endometriosis remain poorly defined. Downregulated 3'-tRFAlaAGC validated from endometrial lesions and serum was demonstrated to suppress the invasion of endometriosis. Indeed, we identified that nuclear translocation of p65 mediated by MCCC1 protein was attenuated due to the occurrence of 3'-tRFAlaAGC-MCCC1 compound relying on the 383-494aa of MCCC1, a unique binding site where 3'-tRFAlaAGC directly bond to MCCC1. Hence, the activation of NF-κB pathway was inhibited, hindering the epithelial-mesenchymal transition related to the progression of endometriosis. Moreover, 3'-tRFAlaAGC alleviated lesion burden in endometriosis mice, and the precious predictive efficiency in serum through the Machine learning. Understanding the 3'-tRFAlaAGC provides a critical opportunity to dissect the mechanisms driving endometriosis progression, opening new avenues to diagnose and halt endometriosis in its tracks.

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