AKIP1 promotes tumor progression by cancer-related pathways and predicts prognosis in tongue squamous cell carcinoma.

The current study was designed to explore the effect of A-kinase-interacting protein 1 (AKIP1) on tongue squamous cell carcinoma (TSCC) viability and mobility and to investigate its molecular mechanism. Control overexpression (OE-NC group) and AKIP1 overexpression (OE-AKIP1 group) plasmids were transfected into CAL-27 cells; control knockdown (KD-NC group) and AKIP1 knockdown (KD-AKIP1 group) plasmids were transfected into SCC-9 cells. Cellular viability and mobility were determined, and mRNA sequencing was performed followed by RT-qPCR validation. Immunohistochemistry was utilized to detect AKIP1 expression in tumor and adjacent tissues from 90 TSCC patients. AKIP1 was more highly expressed in human TSCC cell lines compared to human normal lingual epithelial cells. Cell proliferation, migration, and invasion were increased in the OE-AKIP1 group compared to the OE-NC group but decreased in the KD-AKIP1 group compared to the KD-NC group. mRNA sequencing revealed 436 differentially expressed genes; most of the genes were mainly enriched in the mTOR, PI3K-Akt, MAPK, Hippo, and Wnt signaling pathways. These findings were subsequently confirmed by RT-qPCR quantification. In TSCC patients, AKIP1 expression was increased in tumor tissues and related to increased tumor size, lymph node metastasis and poor overall survival. AKIP1 is a therapeutic target that regulates multiple tumor-related pathways in TSCC. AJTR