Highly Expressed SPC25 Promotes the Stemness, Proliferation and EMT of Oral Squamous Cell Carcinoma Cells via Modulating the TGF-β Signaling Pathway

Owing to the high incidence of oral squamous cell carcinoma (OSCC), elucidation of its diagnostic and prognostic factors is of great importance. Spindle pole body component 25 (SPC25) is known to play vital roles in different types of cancer. Nevertheless, the role of SPC25 in OSCC has not been elucidated yet. This study aimed to investigate the potential role of SPC25 in OSCC progression via modulating the transforming growth factor beta-1 (TGF-beta 1) signaling pathway. Data showed that SPC25 was highly expressed in oral cancer tumors and cells, which was associated with staging and poor survival of OSCC patients. Silencing of SPC25 was found to inhibit proliferation, colony formation, sternness, and epithelial-mesenchymal transition (EMT) of HSC-3 cells. Further analysis revealed that SPC25 overexpression promoted proliferation, colony formation, sternness, and EMT of OCEM-1 cells. In vivo analysis showed that silencing of SPC25 reduced tumor size, volume, and weight; it also suppressed the expression levels of Ki27, CDK2, vimenrin, and TGF-beta 1. Our findings indicated that SPC25 is crucial for the progression of OSCC, and it modulates proliferation, sternness, and EMT of OSCC cells via regulating the TGF-beta 1 signaling pathway and its associated proteins. This study provided novel insights into the role of SPC25 in the pathogenesis of OSCC, and SPC25 could be a potential therapeutic target for the treatment of OSCC.