CD147 promotes glucose metabolism, invasion and metastasis via PI3K/AKT pathway in oral squamous cell carcinomas

Background: The incidence of oral cancers, especially that of oral squamous cell carcinoma (OSCC), has increased significantly in the last few decades. Aggressive tumor progression and metastasis are the key factors responsible for the high mortality rate associated with OSCC. CD147 is known to play a key role in tumor metastasis and is associated with poor prognosis in oral cancer. It is also a crucial regulator of glucose metabolism in cancer cells. The aim of this study was to determine the effect of CD147 on OSCC invasiveness, metastasis and glucose metabolism, as well as the underlying mechanism. Methods: CD147 was knocked down in the human OSCC lines SCC-25 and CAL-27, and both the wild-type and knockdown cells were then stably transfected with PI3K cDNA. Glucose metabolism and in vitro migration of the OSCC cells were respectively analyzed by glucose uptake and lactate secretion assays, and transwell assay. Results: Knocking down CD147 in the OSCC cells significantly reduced their migration, and decreased glucose metabolism. The inhibitory effects of blocking CD147 were reversed upon PI3K overexpression. Conclusions: CD147 mediates its oncogenic effects via the PI3K/AKT pathway, and is a potential prognostic factor and therapeutic target for OSCC.