Investigation of the Effects of PFKFB3 Small Molecule Inhibitor KAN0438757 on Cell Migration and Expression Level of N-cadherin Protein in Glioblastoma Cell Lines

Authors : Seher Saruhan, Deniz Özdemir, Remziye Safa, Can Ali Agca

Pages : 47-53

Doi:10.46810/tdfd.1385118

View : 261 | Download : 112

Publication Date : 2024-03-26

Article Type : Research Paper

Abstract :PFKFB3 (6-phosphofructose-2-kinase/fructose-2,6-bisphosphatase 3) is a enzyme involved in glycolysis, the process by which cells convert glucose into energy. PFKFB3 is known to be overexpressed in many types of cancer, including glioblastoma, a highly aggressive brain tumour. The epithelial-mesenchymal transition (EMT) is a biological mechanism linked to cancer growth and enhanced invasion and metastasis. Inhibition of PFKFB3 in glioblastoma cells is seen as a potential therapeutic strategy to target EMT and inhibit cancer progression. Various small molecule PFKFB3 inhibitors have been created and tested in preclinical trials. The purpose of this study is to look into the possible effect of KAN0438757, a very efficient PFKB3 inhibitor, on glioblastoma cells. KAN0438757\'s impact on viability of cells, cell migration and cell death in glioblastoma cancer cell lines U373 and U251 were investigated by WST-1 Cell viability, AO/EtBr staining western blotting and wound healing-cell migration assays. Glioblastoma cells showed decreased cell viability and dose-dependent apoptotic morphological changes after KAN0438757 treatment. In addition, it was determined that N-cadherin protein level decreased and cell migration was suppressed. In conclusion, KAN0438757, a PFKFB3 inhibitor, can be considered as a valid approach to target cell death and EMT in glioblastoma cancer cell lines.
Keywords : KAN0438757, PFKFB3, Glioblastoma, Hücre göçü

ORIGINAL ARTICLE URL