BTAF1: a key regulator of DNA end resection and predictor of chemotherapy sensitivity in gastric cancer - PubMed
5 hours ago
- #DNA repair
- #Chemotherapy sensitivity
- #Gastric cancer
- BTAF1 is frequently mutated in gastric cancer and plays a key role in DNA repair.
- BTAF1 knockout leads to accumulation of double-strand breaks (DSBs) by impairing DNA end-resection in homologous recombination (HR) repair.
- BTAF1 prevents ubiquitin-mediated degradation of MRE11, maintaining its stability and promoting HR repair.
- The interaction between BTAF1 and MRE11 is regulated by PARP1-mediated PARylation during DNA damage response.
- Loss of BTAF1 increases chemosensitivity in gastric cancer models, both in vitro and in vivo.
- High BTAF1 expression correlates with poor prognosis in gastric cancer patients receiving neoadjuvant chemotherapy.
- BTAF1 is proposed as a potential biomarker for predicting response to genotoxic chemotherapy.