CUL7-mediated KEAP1 ubiquitination promotes the progression of colon cancer via NRF2 signaling
Le Shi, Feiyu Shi, Yue Zhang, Ruichen Liu, Quanyu Liu, Shuangxi Zhang, Zhen Wang, Wu Su, Dan Gao, Yi Liu, Xiangpeng Dai, Hui Guo, Jiankang Liu, Junjun She, Jiangang Long · 2026
Read CUL7-mediated KEAP1 ubiquitination promotes the progression of colon cancer via NRF2 signaling by Le Shi, Feiyu Shi, Yue Zhang, Ruichen Liu, Quanyu Liu, Shuangxi Zhang, Zhen Wang, Wu Su, Dan Gao, Yi Liu, Xiangpeng Dai, Hui Guo, Jiankang Liu, Junjun She, Jiangang Long (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13462133.txt.
Description
Le Shi and co-authors identify CUL7, a protein tagging enzyme, as a colon cancer accelerator that works by destroying the cell's oxidant guard. High CUL7 marks poor prognosis in patients, but its mechanism was undefined. In their 2026 study, removing CUL7 from colon cancer cells slowed their growth and migration, and adding it back sped both. Mice lacking the gene grew smaller tumors. Molecular work traced the chain to KEAP1, the sensor that normally keeps the antioxidant master switch NRF2 in check.
CUL7 physically binds KEAP1 and tags it for shredding with two chain types, lowering reactive oxygen stress and freeing NRF2 signaling to support growth. The enzyme's tail end proved crucial for controlling KEAP1 stability. Human tumors mirrored the laboratory logic: where CUL7 ran high, KEAP1 ran low and NRF2 high in the clinical correlation analysis. Blocking CUL7's tail interaction is a candidate strategy.
Catalog record
| CREATOR | Le Shi, Feiyu Shi, Yue Zhang, Ruichen Liu, Quanyu Liu, Shuangxi Zhang, Zhen Wang, Wu Su, Dan Gao, Yi Liu, Xiangpeng Dai, Hui Guo, Jiankang Liu, Junjun She, Jiangang Long |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 59 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |