PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20428808-4	2010	In the present study, we found that silibinin treatment resulted in the up-regulation of cytokeratin-18 and down-regulation of vimentin and MMP2, which was consistent with morphologic reversal of EMT phenotype leading to be epithelial.	Silybin	36-45	vimentin	Homo sapiens	127-135	
35189245-8	2022	Also, silibinin reversed the epithelial-mesenchymal transition (EMT) mechanism by inducing E-cadherin expression and reducing N-cadherin and vimentin expression, suppressing the levels of regulators related to EMT such as Snail, Slug, and ZEB1 transcription factors, and also decreasing PI3K/AKT, Smad2/3, and beta-catenin intermediate molecules in vitro.	Silybin	6-15	vimentin	Homo sapiens	141-149	
32748663-6	2021	Silibinin attenuated EMT through decreased expression of N- cadherin and vimentin and increased expression of (E-cadherin).	Silybin	0-9	vimentin	Homo sapiens	73-81	
31612353-5	2020	We here report that silibinin at lower concentrations (30-90 muM) inhibits epithelial to mesenchymal transition (EMT) of MDA-MB-231, by increasing the expression of epithelial marker, E-cadherin, and decreasing the expression of mesenchymal markers, N-cadherin and vimentin.	Silybin	20-29	vimentin	Homo sapiens	265-273	
28926892-15	2017	Western blot results indicated that treated with silibinin alone or in combination of crozitinib for 48 hours, the protein level of E-cadherin in H2228 cells was upregulated, while the expressions of p-ALK and vimentin were downregulated, without obvious alteration of ALK protein expression.	Silybin	49-58	vimentin	Homo sapiens	210-218	
27753543-5	2016	Moreover, silibinin treatment significantly inhibited the upregulation of the immune checkpoint regulator PD-L1 and also EMT regulators (e.g., SLUG, VIM, CD44) in crizotinib-refractory cells.	Silybin	10-19	vimentin	Homo sapiens	149-152	
24012496-5	2013	Mechanistically, silibinin could inhibit glycogen synthase kinase-3beta (GSK3beta) phosphorylation, beta-catenin nuclear translocation and transactivation, and ZEB1 gene transcription that subsequently regulated the expression of cytokeratins, vimentin and matrix metalloproteinase-2 (MMP2) to reverse epithelial-mesenchymal transition (EMT).	Silybin	17-26	vimentin	Homo sapiens	244-252	
23764119-2	2013	METHODS: The effect of silibinin on the expression of alpha-smooth muscle actin (alpha-SMA) and vimentin in response to transforming growth factor-beta1 (TGF-beta1) was determined in human tenon fibroblasts (HTFs).	Silybin	23-32	vimentin	Homo sapiens	96-104	
19578386-0	2009	Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression.	Silybin	0-9	vimentin	Homo sapiens	83-91	
19578386-11	2009	Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose- and time-dependent manner after treatment of silibinin.	Silybin	148-157	vimentin	Homo sapiens	31-39	
19578386-12	2009	CONCLUSION: This study shows that silibinin could inhibit the invasion, motility and migration of ARCaP(M) cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.	Silybin	34-43	vimentin	Homo sapiens	136-144