Rui Wang - Department of Otolaryngology-Head and Neck Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi, ۰۳۰۰۳۲, China
Ying Gao - Department of Otolaryngology-Head and Neck Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi, ۰۳۰۰۳۲, China
Huimin Zhang - Department of Otolaryngology-Head and Neck Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi, ۰۳۰۰۳۲, China

Objective(s): The aim of this study was to detect the expression levels of α-Actinin ۱ (ACTN۱) and ITGA۵ in HNSCC and to explore how ACTN۱/ITGA۵ regulated the proliferative and invasive abilities, as well as the EMT of Head and neck squamous cell carcinoma (HNSCC) cells. Materials and Methods: The viability, proliferative, invasive and migrative abilities of HNSCC cells after transfection were, in turn, detected by CCK‑۸ assay, colony formation assay, EdU staining, transwell, as well as wound healing. E-cadherin in transfected cells was assessed utilizing immunofluorescence. RT-qPCR confirmed the transfection effect of ACTN۱ and ITGA۵ in HNSCC cells and the interaction between ACTN۱ and ITGA۵ in HNSCC cells was determined by co-immunoprecipitation (Co-IP). With Western blot application, the contents of ACTN۱, ITGA۵, proliferation-, invasion- and migration-related proteins were estimated. A xenograft model based on nude mice was conducted and Ki-۶۷ content in tumor tissues was evaluated employing immunohistochemistry (IHC) staining.Results: ACTN۱ interacted with ITGA۵. The contents of ACTN۱ and ITGA۵ were found to be abundant in HNSCC tissues and cells and associated with poor prognosis. ACTN۱ depletion imparted suppressive impacts on cell proliferative, invasive and migrative abilities as well as EMT of HNSCC cells, which were reversed by ITGA۵ overexpression. In addition, ACTN۱ deficiency repressed the growth and metastasis of tumor tissues in tumor xenografts of nude mice. Conclusion: ACTN۱ positively interacts with ITGA۵ to promote proliferation, invasion and EMT of HNSCC cells. Also, ACTN۱ promotes tumor growth and metastasis.

ACTN۱, Epithelial-mesenchymal transformation, Head and neck squamous cell carcinomas, Invasion ITGA۵