PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32562663-0	2020	Sirt3 promotes hepatocellular carcinoma cells sensitivity to regorafenib through the acceleration of mitochondrial dysfunction.	regorafenib	61-72	sirtuin 3	Homo sapiens	0-5	
32562663-4	2020	This study aimed to investigate the mechanism of Sirt3 involved in the mitochondrial dysfunction which associated with regorafenib treatment in liver cancer cells.	regorafenib	119-130	sirtuin 3	Homo sapiens	49-54	
32562663-5	2020	We found regorafenib inhibited Sirt3 and p-ERK expression in HCC cells in a dose-dependent manner.	regorafenib	9-20	sirtuin 3	Homo sapiens	31-36	
32562663-7	2020	After transfected with Sirt3 overexpression plasmid, we found that Sirt3 sensitized liver cancer cells to regorafenib and resulted in much more apoptosis with a significant increase of ROS level.	regorafenib	106-117	sirtuin 3	Homo sapiens	23-28	
32562663-7	2020	After transfected with Sirt3 overexpression plasmid, we found that Sirt3 sensitized liver cancer cells to regorafenib and resulted in much more apoptosis with a significant increase of ROS level.	regorafenib	106-117	sirtuin 3	Homo sapiens	67-72	
32562663-9	2020	Mitochondrial membrane potential assay indicated that Sirt3 overexpression accelerated the mitochondrial depolarization process induced by regorafenib and aggravated mitochondrial injury.	regorafenib	139-150	sirtuin 3	Homo sapiens	54-59	
32562663-11	2020	The results demonstrated that Sirt3 overexpression promoted the increase of ROS and apoptosis induced by regorafenib through the acceleration of mitochondrial dysfunction by impairing function of the electron transport chain in liver cancer cells.	regorafenib	105-116	sirtuin 3	Homo sapiens	30-35	
32562663-12	2020	Our studies verified the functional role of Sirt3 in regorafenib treatment and suggested that regorafenib accompanied with Sirt3 activator as a novel treatment strategy for HCC.	regorafenib	53-64	sirtuin 3	Homo sapiens	44-49