LDHC4 drives lung adenocarcinoma progression by inducing lactylation of RB1 at lysine 900 to disrupt the RB1–E2F1 complex
Wei Peng, Zhi Lin, Cheng Sun, Lingjing Lin, Zhaolei Cui, Donghong Lin · 2026
Read LDHC4 drives lung adenocarcinoma progression by inducing lactylation of RB1 at lysine 900 to disrupt the RB1–E2F1 complex by Wei Peng, Zhi Lin, Cheng Sun, Lingjing Lin, Zhaolei Cui, Donghong Lin (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-13156858.txt.
Description
Wei Peng and co-authors trace in 2026 how a metabolic enzyme fuels the commonest lung cancer. The enzyme, LDHC4, runs high in lung adenocarcinoma and marks poor survival, but its tricks beyond sugar burning were unclear. The team checked tumor databases, ninety paired tissue samples, and cell models where the enzyme was raised or cut.
The culprit is a chemical tag, lactylation, that the enzyme promotes on the tumor guard RB1 at one exact site. The tag breaks RB1's grip on its partner E2F1, freeing the cell cycle. Blocking the site reversed the effect in tests. The study names the enzyme a prognostic risk factor and a possible drug target.
Catalog record
| CREATOR | Wei Peng, Zhi Lin, Cheng Sun, Lingjing Lin, Zhaolei Cui, Donghong Lin |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 65 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |