TRPC1能够调节肿瘤的生长和浸润，但是它在舌鳞状细胞癌（TSCC）中的作用尚不清楚。本研究旨在探讨TRPC1敲低对TSCC细胞功能的影响及其潜在的分子机制。将TSCC细胞系转染TRPC1或阴性对照小干扰核糖核酸，然后进行PI3K激活剂的孵育。与对照组相比，TSCC细胞系（包括SCC-15、CAL-33、HSC-3和YD-15）中TRPC1呈显著上调（均P < 0.05）。由于SCC-15和YD-15细胞中TRPC1表达明显上调，因此选择它们进行进一步的研究。TRPC1敲低既能在YD-15细胞中又能在SCC-15细胞中抑制细胞增殖（48小时和72小时均P < 0.05）、促进凋亡（均P < 0.05）和抑制浸润（均P < 0.05）。同时，TRPC1敲低能够减弱磷脂肌醇3-激酶和蛋白激酶B的磷酸化水平（均P < 0.05）。此外，PI3K激活剂能够减弱TRPC1敲低对细胞增殖、凋亡和浸润的影响（均P < 0.05）。TRPC1被认为是TSCC治疗的潜在靶点，其敲低能够通过使PI3K/AKT通路失活来抑制生长和浸润。

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.TSCC cell lines were transfected with TRPC1 or negative control small interfering ribonucleic acids, and then PI3K activator was incubated after transfection.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).TRPC1 shows potential as a candidate treatment target, whose knockdown inhibits growth and invasion through inactivating PI3K/AKT pathway in TSCC.