Title : Inhibition of the IGF signaling pathway reverses cisplatin resistance in ovarian cancer cells.

Pub. Date : 2017 Dec 14

PMID : 29241458






5 Functional Relationships(s)
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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