PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33681180-0	2020	Metformin Resensitizes Sorafenib-Resistant HCC Cells Through AMPK-Dependent Autophagy Activation.	Sorafenib	23-32	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	61-65	
33681180-5	2020	We further found that the resistance of EGFR-overexpressed liver cancer cells to sorafenib is associated with low activity of AMP-activated protein kinase (AMPK) and CCAAT/enhancer binding protein delta (CEBPD) as well as insufficient autophagic activation.	Sorafenib	81-90	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	126-154	
33681180-5	2020	We further found that the resistance of EGFR-overexpressed liver cancer cells to sorafenib is associated with low activity of AMP-activated protein kinase (AMPK) and CCAAT/enhancer binding protein delta (CEBPD) as well as insufficient autophagic activation.	Sorafenib	81-90	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	156-160	
33681180-7	2020	Moreover, treatment with metformin can increase sorafenib sensitivity through AMPK activation in EGFR-overexpressed liver cancer cells.	Sorafenib	48-57	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	78-82	
33681180-8	2020	This study suggests that AMPK/CEBPD-activated autophagy could be a potent strategy for improving the efficacy of sorafenib in HCC patients.	Sorafenib	113-122	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	25-29