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