PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29241458-9	2017	IGF1, IGF1R, AKT p-IGF1, p-IGF1R, and p-Akt protein expression was enhanced dose-dependently with metformin, and was also significantly changed by treatment of CP70 cells with 0 mM metformin +10 mM LY294002.	Metformin	98-107	AKT serine/threonine kinase 1	Homo sapiens	13-16	
29241458-9	2017	IGF1, IGF1R, AKT p-IGF1, p-IGF1R, and p-Akt protein expression was enhanced dose-dependently with metformin, and was also significantly changed by treatment of CP70 cells with 0 mM metformin +10 mM LY294002.	Metformin	98-107	AKT serine/threonine kinase 1	Homo sapiens	40-43	
29241458-9	2017	IGF1, IGF1R, AKT p-IGF1, p-IGF1R, and p-Akt protein expression was enhanced dose-dependently with metformin, and was also significantly changed by treatment of CP70 cells with 0 mM metformin +10 mM LY294002.	Metformin	181-190	AKT serine/threonine kinase 1	Homo sapiens	13-16	
29241458-10	2017	Moreover, changes in the expression of MRP2, IGF1, IGF1R, and AKT was metformin-concentration dependent, and was significantly different from that in the untreated control group (P < 0.05).	Metformin	70-79	AKT serine/threonine kinase 1	Homo sapiens	62-65	
29241458-12	2017	CONCLUSION: Metformin can improve the sensitivity of ovarian cancer CP70 cells to cisplatin in a concentration-dependent manner by activating the AKT signaling pathway, inhibiting the IGF1R signaling pathway, and reducing MRP2 expression.	Metformin	12-21	AKT serine/threonine kinase 1	Homo sapiens	146-149