STT3 promotes cervical cancer proliferation and apoptosis via PI3K/AKT pathway.

BACKGROUND: The catalytic subunit of the oligosaccharyltransferase (OST) complex, STT3, is essential for protein glycosylation. STT3 is implicated in several cancers; however, its roles in the progression of cervical cancer (CC) have not been clarified. METHODS: Immunohistochemical staining for STT3 was performed on 102 human CC tissue samples. We analyzed the association of these OST complex subunits with overall survival and progression-free survival in patients with CC. STT3 expression in CC cells was manipulated using downregulation vectors and the inhibitor NGI-1. EdU assay, CCK-8 assay, plate cloning assay, flow cytometric analysis, TUNEL assay, scratch healing assay, and Transwell assay were used to assess the proliferation, apoptosis, and migration of tumor cells. A subcutaneous xenograft tumor model in mice was established to monitor tumor growth. The association between STT3 and the PI3K/AKT pathway was analyzed using the TCGA database and GSEA tool. RESULTS: High expression levels of STT3 were associated with lower survival rates in patients with CC. Downregulation of STT3 inhibited the proliferation, migration, and invasion of CC cells in vitro and promoted apoptosis of tumor cells. Additionally, STT3 was found to modulate the PI3K/AKT pathway and the epithelial-mesenchymal transition (EMT) process, thereby influencing CC cell progression. Treatment with the PI3K/AKT pathway activator 740 Y-P partially reversed the tumor-suppressive effects of STT3 downregulation in vitro. CONCLUSION: STT3 expression in CC cells exerts a pro-tumorigenic effect. STT3A and STT3B regulate the PI3K/AKT pathway and EMT process, thereby affecting tumor progression.