RETSAT associates with DDX39B to promote fork restarting and resistance to gemcitabine based chemotherapy in pancreatic ductal adenocarcinoma.

Qiu TuXiuyun LiuXiaoqing YaoRuixue LiGaojing LiuHonglv JiangKaiqin LiQiongfang ChenXiaoyan HuangQing ChangGuoqiang XuHong ZhuPeng ShiBo Zhao

Published in: Journal of experimental & clinical cancer research : CR (2022)

This study identified RETSAT as a novel replication fork protein, which functions through interacting with DDX39B mediated R-loop clearance to promote fork restarting, leading to cellular resistance to replication stresses co-induced by tumor environmental hypoxia and gemcitabine in pancreatic ductal adenocarcinoma.

Keyphrases

locally advanced
rectal cancer
endothelial cells
transcription factor
protein protein
binding protein
climate change
risk assessment
small molecule
chemotherapy induced