The Proliferation of Glioblastoma Is Contributed to Kinesin Family Member 18A and Medical Data Analysis of GBM

Abstract

Background: Glioblastoma (GBM) is widely known as a classical kind of malignant tumor originating in the brain with high morbidity and mortality. Targeted therapy has shown great promise in treating glioblastoma, but more promising targets, including effective therapeutic targets, remain to be identified. 18A (KIF18A) is a microtubule-based motor protein that is dysregulated and involved in the progression of multiple human cancers. However, the possible effects of KIF18A on GBM progression are still unclear.Methods: We performed DEG analysis, medical data analysis, and network analysis to identify critical genes affecting glioma progression. We also performed immunohistochemical analysis of the KIF18A levels in 94 patients with glioblastoma and the associated surrounding tissues. Patients were divided into two groups according to the high and low expression. Using a clinical analysis, we showed the potential associations between KIF18A expression and clinical characteristics of 94 GBM patients. We then investigated the effects of KIF18A on GBM cell proliferation by colony establishment, MTT, and immune blogging. The possible effect of KIF18A on GBM tumor growth was determined in mice.Results: We identified KIF18A as a potential gene affecting GBM progression. We further demonstrated that GBM tissues expressed KIF18A much higher, and its presentation was associated with recurrence in glioblastoma patients. We believe KIF18A promotes GBM cell proliferation.Conclusion: We demonstrated that KIF18A could be a promising target in treating GBM.

Crebanine, an aporphine alkaloid, induces cancer cell apoptosis through PI3K-Akt pathway in glioblastoma multiforme

“…In addition, NGS showed a significant decrease in the gene expression of base excision repair and motor proteins. This decrease may undermine GBM cells’ ability to function normally, collaboratively reducing the viability and proliferation of GBM ( Poletto et al, 2017 ), especially given that kinesin family members, the motor proteins downregulated in the result of NGS, have been found to be connected to and even advantageous for the proliferation of GBM cells ( Wang L. B. et al, 2022 ; Wang L. et al, 2022 ). NGS has revealed several anti-cancer mechanisms for the CB treatment of GBM cells.…”

KIF18A improves migration and invasion of colorectal cancer (CRC) cells through inhibiting PTEN signaling

“…Additionally, KIF18 interacts with tumors to inhibit p53, exhibiting a potential regulatory role in cancer progression. Current studies have uncovered that KIF18A has a high expression in many human tumors, including CRC [29][30][31][32]. However, its functional molecular mechanisms in CRC have not been fully explored.…”

KIF18A interacts with PPP1CA to promote the malignant development of glioblastoma

“…Stangeland et al (9) showed that KIF18A can be a potential therapeutic target for GBM. A relevant clinical study demonstrated that KIF18A expression is higher in human GBM tissues than normal tissues, and its expression is closely associated with the recurrence of GBM in patients (10). However, to the best of our knowledge, the specific mechanism of KIF18A in GBM has not been yet elucidated.…”