![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
Preview |
PDF (Preprint)
- Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
20MB |
| Item Type: | Preprint |
|---|---|
| Title: | Interferon-independent STING enforces epithelial genome-integrity checkpoint to restrain tumor evolution |
| Creators Name: | Xiang, Hang, Macino, Martina, Woitaske-Proske, Clemens, Bodenstein, Nicholas, Bernardes, Joana P., Tran, Florian, Schmid, Nicole A., Martini, Gabriela Rios, Wotawa, Felix, Bornhaeuser, Johanna, Kakavand, Nassim, Dyck Dionisi, Oliver, van den Bossche, Silke, Yang, Guang, Wu, Qicong, Kugler, Julia, Welz, Lina, Konukiewitz, Bjorn, Fischer, Julius C., Peifer, Christian, Schreiber, Stefan, Rosenstiel, Philip, Tschurtschenthaler, Markus, Sanders, Ashley D. and Aden, Konrad |
| Abstract: | STING is canonically known for mediating interferon responses to cytosolic DNA, yet its cell-intrinsic role in genome maintenance beyond the immune context is unknown. Here we show that epithelial STING functions as a type I interferon-independent genome-integrity checkpoint. STING loss impairs homologous recombination repair, attenuates ATM-associated damage signaling, elevates CDK1 activity, and causes chromosomal instability revealed by single-cell Strand-seq, culminating in spontaneous intestinal adenocarcinoma. These defects arise before tumor formation and confer selective vulnerability to CDK inhibition in tumor organoids and human colorectal cancer cells. Our findings identify STING as a cell-autonomous guardian of epithelial genome stability that restrains chromosomal instability-driven tumor evolution beyond its canonical immune function. |
| Keywords: | Animals, Mice |
| Source: | bioRxiv |
| Publisher: | Cold Spring Harbor Laboratory Press |
| Article Number: | 2026.02.17.706442v2 |
| Date: | 25 March 2026 |
| Official Publication: | https://doi.org/10.64898/2026.02.17.706442 |
Repository Staff Only: item control page
