The Comparative Mechanism of KP-10 Pre-Treatment Towards Temozolomide Induced Autophagy and Apoptosis Mediated DNA Damage in Human Glioblastoma Cells.

Finding effective drug targets for glioblastoma (GBM) is a challenge, primarily due to the high level of acquired resistance to temozolomide (TMZ) . KISSIR (activated by kisspeptin), also known as GPR54, is reported to modulate the response of chemotherapy drugs in various cancer types, however its role in GBM response to TMZ remains unknown. Therefore, this study aim was to investigate the underlying mechanism(s) through which kisspeptin/KISS1R in modulating TMZ activity in KISS1R-expressing GBM cells. This study sheds the light on the dynamic action of KP-10/TMZ on various mechanisms related to TMZ resistance such as cell cycle arrest, autophagy, DNA damage and apoptosis . The identification of KP-10/KISS1R as a potential therapeutic target expands our knowledge of its role in GBM treatment response, emphasizing the need for further exploration of the intricate mechanisms uncovered in this study.