PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18374204-3	2008	Our laboratory findings revealed that the inhibitory effect of vitamin K2 against HCC cell growth was generated by suppressing cyclin D1 expression through inhibition of NF-kappaB activation.	Vitamin K 2	63-73	cyclin D1	Homo sapiens	127-136	
17404108-5	2007	A reporter gene assay of the cyclin D1 promoter was done under vitamin K2 treatment.	Vitamin K 2	63-73	cyclin D1	Homo sapiens	29-38	
17404108-8	2007	RESULTS: Vitamin K2 inhibited cyclin D1 mRNA and protein expression in a dose-dependent manner in the HCC cells.	Vitamin K 2	9-19	cyclin D1	Homo sapiens	30-39	
17404108-9	2007	Vitamin K2 also suppressed the NF-kappaB binding site-dependent cyclin D1 promoter activity and suppressed the basal, 12-O-tetradecanoylphorbol-13-acetate (TPA)-, TNF-alpha-, and interleukin (IL)-1-induced activation of NF-kappaB binding and transactivation.	Vitamin K 2	0-10	cyclin D1	Homo sapiens	64-73	
17404108-11	2007	Moreover, HCC cells overexpressing cyclin D1 and p65 became resistant to vitamin K2 treatment.	Vitamin K 2	73-83	cyclin D1	Homo sapiens	35-44	
17404108-12	2007	CONCLUSION: Vitamin K2 inhibits the growth of HCC cells via suppression of cyclin D1 expression through the IKK/IkappaB/NF-kappaB pathway and might therefore be useful for treatment of HCC.	Vitamin K 2	12-22	cyclin D1	Homo sapiens	75-84	
15703828-8	2005	Protein expression of cyclin D1 and cyclin-dependent kinase 4 (Cdk4), but not p16INK4a Cdk inhibitor in the tumor was significantly reduced by vitamin K2 or K3 treatment, indicating that vitamins K2 and K3 may induce G1 arrest of cell cycle on PLC/PRF/5 cells in vivo.	Vitamin K 2	143-153	cyclin D1	Homo sapiens	22-31