Pub. Date : 2017 Dec 14
PMID : 29241458
5 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | 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 | AKT serine/threonine kinase 1 | Homo sapiens |
2 | 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 | AKT serine/threonine kinase 1 | Homo sapiens |
3 | 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 | AKT serine/threonine kinase 1 | Homo sapiens |
4 | 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 | AKT serine/threonine kinase 1 | Homo sapiens |
5 | 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 | AKT serine/threonine kinase 1 | Homo sapiens |