PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34150623-6	2021	Lovastatin inhibited EMT as demonstrated by down-regulation of the protein levels of Vimentin and Twist in MDA-MB-231 CSCs in vitro and vivo and by reversal of TGF-beta1-induced morphological change in MCF10A cells.	Lovastatin	0-10	transforming growth factor beta 1	Homo sapiens	160-169	
18287089-6	2008	Lovastatin and a geranylgeranyltransferase inhibitor reduce the TGFbeta1-stimulated levels of CCN2/CTGF protein by approximately 75 and 100%, respectively.	Lovastatin	0-10	transforming growth factor beta 1	Homo sapiens	64-72	
23485731-6	2013	We demonstrate that the intensity of FMT induced by TGF-beta1 was strongly and dose-dependently attenuated by lovastatin.	Lovastatin	110-120	transforming growth factor beta 1	Homo sapiens	52-61	
23485731-9	2013	Additionally we demonstrate that in bronchial fibroblast populations, both inhibitors (lovastatin and zaragozic acid A) attenuate the TGF-beta1-induced Smad2 nuclear translocation in a manner dependent on intracellular cholesterol level.	Lovastatin	87-97	transforming growth factor beta 1	Homo sapiens	134-143	
31079432-11	2019	Results: Simultaneous or sequential treatment of TGF-beta1 and lovastatin could further augment the BMP-2 overexpression compared with lovastatin-alone treatment.	Lovastatin	135-145	transforming growth factor beta 1	Homo sapiens	49-58	
31079432-14	2019	Cells in groups treated with lovastatin were less populated than that in the group treated with TGF-beta1 alone.	Lovastatin	29-39	transforming growth factor beta 1	Homo sapiens	96-105	
26517522-5	2016	While Lovastatin"s inhibitory effects on TGFbeta1, COX2, and ICAM-1 expression were independently controlled by the tumor suppressor LKB1, integrin beta3 expression was not affected.	Lovastatin	6-16	transforming growth factor beta 1	Homo sapiens	41-49	
22129737-3	2011	In the present study, probucol and lovastatin, which are therapeutics used for hyperlipidemia and proposed to act as anti-oxidants, were examined in terms of their effect on TGFbeta1-induced formation of ROS and expression of alpha-smooth muscle actin (alphaSMA), a myofibroblast marker, in human fetal lung fibroblasts (HFL1 cells).	Lovastatin	35-45	transforming growth factor beta 1	Homo sapiens	174-182	
22129737-5	2011	Treatment with probucol (30 microM) and lovastatin (1 microM and 3 microM), in addition to lecithinized-SOD, significantly inhibited the TGFbeta1-induced formation of ROS and alphaSMA.	Lovastatin	40-50	transforming growth factor beta 1	Homo sapiens	137-145	
18421080-0	2008	Lovastatin inhibits TGF-beta-induced myofibroblast transdifferentiation in human tenon fibroblasts.	Lovastatin	0-10	transforming growth factor beta 1	Homo sapiens	20-28	
18421080-3	2008	HMG-CoA-reductase inhibitors (statins) have been shown to inhibit Rho-GTPase signaling; therefore, the authors studied the influence of lovastatin on TGF-beta-mediated myofibroblast transdifferentiation to assess the potential use of statins in wound healing modulation.	Lovastatin	136-146	transforming growth factor beta 1	Homo sapiens	150-158	
18421080-9	2008	RESULTS: Lovastatin inhibited TGF-beta-induced CTGF transcription, alpha-SMA expression and incorporation into actin stress fibers, and subsequent collagen gel contraction.	Lovastatin	9-19	transforming growth factor beta 1	Homo sapiens	30-38	
18421080-12	2008	Lovastatin decreased TGF-beta-induced p38 activation, whereas Smad-2/3 phosphorylation and nuclear translocation were preserved.	Lovastatin	0-10	transforming growth factor beta 1	Homo sapiens	21-29	
18421080-13	2008	CONCLUSIONS: Lovastatin inhibits TGF-beta-induced myofibroblast transdifferentiation in human Tenon fibroblasts, most likely by interfering with Rho-signaling.	Lovastatin	13-23	transforming growth factor beta 1	Homo sapiens	33-41	
18061125-8	2008	These results indicate that lovastatin prevents the Ox-LDL-induced Ras/ERK activation that results in inhibition of Smad3 activation in mesangial cells with subsequent downregulation of TGF-beta target genes.	Lovastatin	28-38	transforming growth factor beta 1	Homo sapiens	186-194	
18061125-5	2008	Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity.	Lovastatin	143-153	transforming growth factor beta 1	Homo sapiens	255-264