TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway
Xin Lai, Jin Zhu, Haocheng Jia, Ping Zhang, Bin Wang, Yuping Tang, Qishan Ran · 2026
Read TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway by Xin Lai, Jin Zhu, Haocheng Jia, Ping Zhang, Bin Wang, Yuping Tang, Qishan Ran (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/PMC13461843.txt.
Description
Xin Lai and colleagues report, in a 2026 laboratory study, that the protein TRIM47 helps glioma tumors grow and resist cell death. Glioma is among the most aggressive brain tumors, with a poor outlook. The team measured TRIM47 in tumor tissue and glioma cells grown in the lab. They lowered or raised its levels to watch changes in cell growth, energy use, and survival signals.
Tumor tissue and cell lines held more TRIM47 than normal. High levels went with shorter survival in the most severe glioma form. Cutting TRIM47 slowed cell growth, stalled the cycle, raised cell death, and shifted energy use away from sugar burning. Raising it did the reverse. A drug blocking a survival pathway, NF-kappaB, undid those gains, tying the effect to that pathway. In mice, tumors with lowered TRIM47 grew smaller and lighter. The authors name TRIM47 as a drug target for glioma.
Catalog record
| CREATOR | Xin Lai, Jin Zhu, Haocheng Jia, Ping Zhang, Bin Wang, Yuping Tang, Qishan Ran |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 34629 |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |