CIP2A interacts with AKT1 to promote the malignant biological behaviors of oral squamous cell carcinoma by upregulating the GSK‑3β/β‑catenin pathway

Oral squamous cell carcinoma (OSCC) is one of the most common malignancies worldwide, which associated with a poor prognosis. The present study aimed to investigate role cancerous inhibitor protein phosphatase 2A (CIP2A) in OSCC and its regulatory effect on AKT1. Firstly, CIP2A AKT1 expression cells was detected by western blotting. After silencing CIP2A, viability proliferation were assessed using Cell Counting Kit‑8 assay 5‑ethynyl‑2'‑deoxyuridine staining. apoptosis evaluated TUNEL staining apoptosis‑related proteins Wound healing, Transwell tube formation assays performed evaluate CAL‑27 migration, invasion human umbilical vein endothelial (HUVEC) formation. interaction between identified co‑immunoprecipitation (co‑IP). In addition, overexpressed CIP2A‑silenced perform rescue experiments analyze malignant biological functions cells. Finally, glycogen synthase kinase (GSK)‑3β/β‑catenin pathway determined blot analysis. Markedly elevated observed knockdown inhibited viability, proliferation, migration invasion, promoted Concurrently, loss‑of‑function attenuated Results Co‑IP confirmed there an Rescue suggested that overexpression alleviated inhibitory effects cells, as well HUVECs . Additionally, significantly downregulated phosphorylated‑GSK‑3β β‑catenin expression, reversed overexpression. conclusion, could interact promote behaviors upregulating GSK‑3β/β‑catenin pathway. These findings may provide targeted therapy for treatment.