ASPM combined with KIF11 promotes the malignant progression of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway

To investigate the molecular mechanism of assembly factor for spindle microtubules (ASPM) in the regulation of the malignant progression of hepatocellular carcinoma (HCC), bioinformatics analysis was utilized to analyze the role of ASPM in the malignant progression of HCC and its potential interaction with the kinesin family member 11 (KIF11) gene. The expression levels of ASPM and KIF11 were detected by reverse transcription-quantitative PCR and western blotting. Following knockdown of ASPM expression, Cell Counting Kit-8/colony formation assays were performed to detect cell viability and proliferation. Wound healing and Transwell assays were employed to detect cell migration and invasion. Additionally, a co-immunoprecipitation (CO-IP) assay was used to detect whether there was an interaction between ASPM and KIF11. KIF11 overexpression was performed to verify if ASPM exerted its effects via KIF11. ASPM was highly expressed in HCC tissues and cells, and was closely associated with a poor prognosis of patients with HCC. Interference with ASPM expression markedly inhibited the viability, proliferation, invasion and migration of HCC cells. Using a CO-IP assay, it was revealed that there was an interaction between ASPM and KIF11. Rescue experiments subsequently revealed the regulatory effects of ASPM on the activity, proliferation, invasion and migration of HCC cells via KIF11. Finally, western blot analysis demonstrated that ASPM in combination with KIF11 promoted the malignant progression of HCC by regulating the activity of the Wnt/beta-catenin signaling pathway. Therefore, the present study demonstrated that ASPM may interact with KIF11 in HCC cells to promote the malignant progression of HCC via the Wnt/beta-catenin signaling pathway.