PT - JOURNAL ARTICLE AU - TAE-HUN KIM AU - JI HYE YOON AU - SUNG-GOOK CHO TI - Kisspeptin Promotes Glioblastoma Cell Invasiveness <em>Via</em> the Gq-PLC-PKC Pathway AID - 10.21873/anticanres.13942 DP - 2020 Jan 01 TA - Anticancer Research PG - 213--220 VI - 40 IP - 1 4099 - http://ar.iiarjournals.org/content/40/1/213.short 4100 - http://ar.iiarjournals.org/content/40/1/213.full SO - Anticancer Res2020 Jan 01; 40 AB - Background/Aim: Kisspeptin produced from the KISS1 gene is secreted from the living cells, binds to endogenous receptor KISS1R (also called G protein-coupled receptor 54, GPR54), and has various functions in normal physiological conditions. Although an anti-metastatic role of kisspeptin in cancer is well known in several cancer types, its role in brain tumors is not yet understood. Herein, we investigated a the role of kisspeptin in glioblastoma cells. Materials and Methods: Glioblastoma cells were treated with kisspeptin and subjected to proliferation, migration, and invasion assays. KISS1R dependency was tested by KISS1R silencing with KISS1R siRNAs. Results: Kisspeptin inhibited migratory and invasive abilities of U87-MG, U-251-MG and U373-MG glioblastoma cells with no effect on cell viability. KISS1R gene silencing with KISS1R siRNAs blocked kisspeptin-induced glioblastoma cell invasiveness. Moreover, chemical inhibitors against Gq, PLC or PKC blocked kisspeptin-induced glioblastoma cell invasiveness. Conclusion: Kisspeptin induces glioblastoma cell invasiveness via the KISS1R-Gq-PLC-PKC signaling pathway.