PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31960187-6	2020	RESULT: This review tries to highlight the effect of itraconazole on smoothened receptor (SMO) in the Hedgehog pathway, thereby reducing the glioma-associated oncogene homolog (GLI) release and finally exhibiting a range of anticancer effects, promoting apoptosis of cancer cells, and inhibiting proliferation by indirect inhibition of NF-kappaB pathway and inflammation, moreover, promoting the expression of cyclin-dependent kinase inhibitors, inhibiting the expression of target genes transcribed by GLI such as BCL-2 and Cyclin-D1.	Itraconazole	53-65	BCL2 apoptosis regulator	Homo sapiens	515-520	
31960187-7	2020	Besides, itraconazole increases the number of Bnip3, subsequently, inducing the dissociation of the Beclin-1/BCL-2 binding complex, as a result of ultimately promoting autophagy of cancer cells.	Itraconazole	9-21	BCL2 apoptosis regulator	Homo sapiens	109-114	
27810405-2	2017	We report that itraconazole was cytotoxic to MCF-7 and SKBR-3 breast cancer cell lines via apoptosis by altering mitochondria membrane potential, reducing BCL-2 expression and elevating caspase-3 activity.	Itraconazole	15-27	BCL2 apoptosis regulator	Homo sapiens	155-160	
31888155-7	2019	At the molecular level, ITR NPs were more effective than ITR solution in inducing pro-apoptotic Bax and p53 while reducing anti-apoptotic Bcl2 protein expression.	Itraconazole	24-27	BCL2 apoptosis regulator	Homo sapiens	138-142	
31888155-7	2019	At the molecular level, ITR NPs were more effective than ITR solution in inducing pro-apoptotic Bax and p53 while reducing anti-apoptotic Bcl2 protein expression.	Itraconazole	57-60	BCL2 apoptosis regulator	Homo sapiens	138-142	
27852416-5	2016	Western blot analysis showed that the Bax, cleaved-caspase 3 expression of itraconazole group and itraconazole+ PDMP group was significantly higher than control group, while Bcl-2 expression was significantly lower than the control; the Bax, cleaved-caspase 3 expression ofitraconazole+ CerS1-shRNA group was significantly lower than itraconazole group, while Bcl-2 expression was significantly higher than the itraconazole group.After 5, 10, 20 mumol/L itraconazole treatment, the expression of p-Akt and p-mTORC1 were significantly lower than the control group; the expression of p-Akt and p-mTORC1 in itraconazole+ CerS-1-shRNA group were significantly higher than itraconazole group.	Itraconazole	75-87	BCL2 apoptosis regulator	Homo sapiens	360-365	
27852416-6	2016	Conclusion: Itraconazole induces apoptosis of PC-3 cell through increasing the intracellular ceramide content, which might relate to upregulation of cleavage-caspase 3 and Bax, downregulation of Bcl-2 and inactivation of Akt-mTORC signal pathway.	Itraconazole	12-24	BCL2 apoptosis regulator	Homo sapiens	195-200