Abstract
CD90, also known as Thy-1 cell surface antigen, is located on human chromosome 11q23.3, and encodes a glycosylphosphatidylinositol-linked cell surface glycoprotein. CD90 serves a key role in malignancy by regulating cell proliferation, metastasis and angiogenesis. Gastric cancer is one of the most common types of malignancy. Patients with advanced gastric cancer have a poor prognosis. CD90 plays a key role in the occurrence and progression of gastric cancer. However, the molecular mechanism of CD90 in gastric cancer is currently unclear. In order to identify the molecular mechanism by which CD90 affects the biological behavior and energy metabolism of gastric cancer cells, the present study used Cell Counting Kit-8 assays, lactate concentration determination and ATP content determination. The results demonstrated that CD90 promotes proliferation and inhibits senescence in gastric cancer cells. In addition, CD90 enhanced the invasion and migration abilities of AGS gastric cancer cells. Overexpression of CD90 resulted in the accumulation of intracellular lactic acid in AGS cells. CD90 upregulated lactate dehydrogenase levels and increased the NADPH/NADP+ ratio in AGS cells. CD90 overexpression decreased the ATP concentration in AGS cells. PI3K, PDK1, phosphorylated-AKT-Ser473, HIF-1α, MDM2 and SIRT1 levels were upregulated in CD90-overexpressing AGS cells, compared with AGS cells transfected with the empty vector. In contrast, PTEN, p53, SIRT2, SIRT3 and SIRT6 were downregulated. The results indicate that CD90 affects the biological behavior and levels of energy metabolism of gastric cancer cells by targeting the PI3K/AKT/HIF-1α signaling pathway.