Aurora-A Regulating Cervical Cancer Invasion and Metastasis through ARPC4

Abstract

Abstract Objective：To investigate the impact of ARPC4 knockdown on cervical cancer cells with Aurora-A overexpression in terms of proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Methods:Gene expression profiling by RNA-seq, qPCR, and Western blotting were used to identify genes potentially regulated by Aurora-A. The proliferation, migration, and invasion abilities of the control and experimental groups were assessed using EDU fluorescence detection, cloning, scratch, and transwell assays. The molecular mechanism underlying ARPC4 regulation by Aurora-A was explored using Western blot analysis. Results:ARPC4 expression was found to decrease in Aurora-A knockdown cells and increase in Aurora-A overexpression cells. Patients with high ARPC4 expression had significantly shorter overall survival compared to those with low expression. Knockdown of ARPC4 counteracted the proliferation of cervical cancer cells induced by Aurora-A overexpression. Migration and invasion capabilities were suppressed in Aurora-A overexpression cell lines following ARPC4 knockdown. Aurora-A activation of the NF-κB p65 signaling pathway led to an upregulation of ARPC4 expression. Conclusion:ARPC4 expression is regulated by Aurora-A, and its knockdown mitigates the effects of Aurora-A overexpression on cervical cancer cells. Aurora-A activation of the NF-κB p65 signaling pathway upregulates ARPC4 expression, providing a potential therapeutic target for cervical cancer treatment.