Pim-1 (Provirus integration site for Moloney murine leukemia virus 1) belongs to the Ser/Thr kinase family and plays a pivotal role in occurrence and development of oncogenesis. Recent studies have demonstrated that Pim-1 phosphorylates RUNX3 and alters its subcellular localization. As a highly malignant tumor, salivary adenoid cystic carcinoma (ACC) accounts for approximately 10% of all epithelial salivary tumors and the 5-year survival rate of patients with highly metastatic ACC is less than 20%. However, few studies have concerned the implications of Pim-1 in the salivary ACC.
In this study, we aimed to clarify the function of Pim-1 in ACC cell lines in vitro. Meanwhile, we measure the levels of Pim-1 and RUNX3 in the ACC tissues. The correlations between Pim-1/RUNX3 levels and clinical parameters were also analyzed.
SACC-83 and SACC-LM cells were transfected with the Pim-1 siRNA. Pim-1 mRNA and protein expression were measured using real-time PCR and immnuoblot, respectively. Cell proliferation was analyzed by CCK-8 assay. Cell cycle, apoptosis, and mitochondrial membrane potential were detected by flow cytometry. Effects of Pim-1 on cells’ invasion were evaluated by transwell migration assay. Pim-1 and RUNX3 levels in ACC tissues were examined by immunohistochemistry.
Pim-1 siRNA reduces cell proliferation, induces apoptosis, causes cell cycle arrest, mitochondrial depolarization, and decreases invasive ability in SACC-83 and SACC-LM cells. Pim-1 and RUNX3 levels are negative relevant and significantly associated with T-stage and nerve invasion in the ACC tissues.
This study demonstrates the oncogenic role of Pim-1 in ACC. The findings also suggest that Pim-1 may serve as a neoteric therapeutic target and potential prognostic marker for ACC cancer.