PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34909649-5	2021	We found that sorafenib upregulated the epithelial marker E-cadherin and downregulated the mesenchymal marker vimentin.	Sorafenib	14-23	cadherin 1	Homo sapiens	58-68	
30272354-6	2018	The combination of capsaicin and sorafenib also inhibited cell invasion and metastasis via upregulation of E-cadherin and downregulation of N-cadherin, vimentin, matrix metalloproteinase (MMP)2 and MMP9.	Sorafenib	33-42	cadherin 1	Homo sapiens	107-117	
32462038-9	2020	Moreover, a knockdown of HOTAIR could improve the therapeutic effect of sorafenib on HCC via increasing E-cadherin and decreasing Vimentin expression.	Sorafenib	72-81	cadherin 1	Homo sapiens	104-114	
28276928-11	2018	We suggest that plectin deficiency and increased E-cadherin in hepatoma cells were associated with higher rates of cell motility, collective cell migration as well as higher drug sensitivity to sorafenib treatment.	Sorafenib	194-203	cadherin 1	Homo sapiens	49-59	
30405889-6	2018	The Notch1-Snail1 signaling pathway contributed to sorafenib resistance via increasing epithelial-mesenchymal transition (EMT) and EMT-mediated cancer stem cell (CSC) features, such as increased expression of Snail1, N-cadherin, ABCG2, and the stem cell related genes Nanog and Oct4, and decreased expression of E-cadherin.	Sorafenib	51-60	cadherin 1	Homo sapiens	312-322	
25862851-6	2015	HGF-stimulated HepG2 cells, which were treated with a combination of sorafenib and vitamin K, showed significantly increased expression of E-cadherin and impairment of migration ability compared to when treated with either agent alone.	Sorafenib	69-78	cadherin 1	Homo sapiens	139-149	
27461522-7	2016	Moreover, the combination of sorafenib and BrMC led to a remarkable decrease in the cellular migration and invasion, the downregulation of N-cadherin protein and upregulation of E-cadherin protein, and increase of cell apoptosis in LCSLCs.	Sorafenib	29-38	cadherin 1	Homo sapiens	178-188	
29021381-4	2017	Results from the initial study demonstrated that sorafenib treatment significantly decreased E-cadherin (P < 0.05) levels but significantly increased matrix metallopeptidase 9 (MMP9) levels (P < 0.01) in A549/SRFres tumors, whereas expression levels of phospho-protein kinase B (AKT), phospho-focal adhesion kinase (FAK), and phospho-Src were elevated in sorafenib-treated A549 and A549/SRFres tumors.	Sorafenib	49-58	cadherin 1	Homo sapiens	93-103	
23724131-12	2013	KRAS transfection of urothelial carcinoma cells led to upregulation of p16(INK4a) and uPA accompanied by loss of E-cadherin that could be inhibited by application of the kinase-inhibitor Sorafenib.	Sorafenib	187-196	cadherin 1	Homo sapiens	113-123	
25447203-11	2015	Long-term treatment with sorafenib decreased E-cadherin, but showed no induction of vimentin expression.	Sorafenib	25-34	cadherin 1	Homo sapiens	45-55