KIF18A interacts with PPP1CA to promote the malignant development of glioblastoma

Glioblastoma (GBM), which has poor prognosis and low 5-year survival rate, is the most common primary central nervous system malignant tumour in adults. Kinesin family member 18A (KIF18A) plays an important role in multiple tumours and is potential therapeutic target for GBM. Therefore, the present study investigated the role of KIF18A in GBM. The expression level and survival prognosis of KIF18A and protein phosphatase 1 catalytic subunit α (PPP1CA) in GBM patients were analysed using the Chinese Glioma Genome Atlas (CGGA) database. Reverse transcription-quantitative PCR and western blot analysis were applied to measure the expression of KIF18A and PPP1CA in normal and GBM cell lines. KIF18A expression was inhibited through cell transfection with a KIF18A-targeting short hairpin RNA. Cell proliferation was detected with the Cell Counting Kit-8 assay. Flow cytometry was used to detect cell cycle changes. Transwell and wound healing assays were used to measure cell invasion and migration. Western blotting was utilized for the detection of invasion- and migration-related proteins MMP9 and MMP2. Biological General Repository for Interaction Datasets and GeneMANIA databases were used to analyse the interaction between KIF18A and PPP1CA. The correlation between PPP1CA and KIF18A was examined using data from the CGGA database. Immunoprecipitation was used to demonstrate the binding relationship between KIF18A and PPP1CA. PPP1CA was overexpressed using cell transfection technology and its mechanism was further examined. The results demonstrated that KIF18A was upregulated in GBM cells compared with normal microglia HMC3. Compared with that in sh-NC group, silencing of KIF18A reduced cell proliferation, induced G(2)/M cycle arrest and inhibited the migration and the invasion of A172 GBM cells by interacting with PPP1CA. In conclusion, KIF18A interacted with PPP1CA to promote the proliferation, cycle arrest, migration and invasion of GBM cells.