PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	45-52	
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	101-108	
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	101-108	
24356455-8	2013	Treatment with 5-AzaC concomitantly upregulated expression of miR-9-3 and miR-193a, and downregulated their respective target genes NF-kappaB and Mcl-1.	Decitabine	15-21	microRNA 9-3	Homo sapiens	62-69	
24356455-11	2013	CONCLUSIONS: Methylation-silencing of miR-9-3 and miR-193a may be an important epigenetic mechanisms favoring NSCLC cell growth and survival for carcinogenesis and cancer progression, and demethylation to reactivate expression of miR-9-3 and miR-193a genes contributes, at least partially, to the anti-cancer properties of 5-AzaC and thereby may be worthy of future studies for the possibility of being a new therapeutic strategy for the treatment of human NSCLCs.	Decitabine	323-329	microRNA 9-3	Homo sapiens	38-45