Abstract

Purpose: Transient receptor potential canonical 1 (TRPC1) modulates tumor growth and invasion, however, its role in tongue squamous cell carcinoma (TSCC) is unclear. The aim of this study was to explore the effect of TRPC1 knockdown on cellular function and its underlying molecular mechanism in TSCC.Methods: TSCC cell lines were transfected with TRPC1 or negative control small interfering ribonucleic acids, and then PI3K activator was incubated after transfection.Results: TRPC1 was elevated in TSCC cell lines (including SCC-15, CAL-33, HSC-3, and YD-15) compared to control cells (all P < 0.05). Since TRPC1 was clearly increased in SCC-15 and YD-15 cells, they were selected for further study. In both YD-15 and SCC-15 cells, TRPC1 knockdown decreased cell proliferation at 48 h and 72 h (all P < 0.05), increased apoptosis (both P < 0.05), and declined invasion (both P < 0.05). Meanwhile, TRPC1 knockdown decreased phosphatidylinositol 3-kinase and protein kinase B phosphorylation (all P < 0.05). Additionally, the effect of TRPC1 knockdown on cell proliferation at 48 h and 72 h, apoptosis, and invasion was attenuated by PI3K activator (all P < 0.05).Conclusion: TRPC1 shows potential as a candidate treatment target, whose knockdown inhibits growth and invasion through inactivating PI3K/AKT pathway in TSCC.