CD300A promotes tumor progression by PECAM1, ADCY7 and AKT pathway in acute myeloid leukemia.

CD300A is a member of the CD300 glycoprotein family of cell surface proteins involved in immune response signaling pathways. There is evidence that CD300A plays a role in autophagy and angiogenesis, while, no studies have been reported which investigated the role of CD300A in tumors. CD300A was found to be highly expressed with statistical significance in acute myeloid leukemia (AML), as well as associated with prognosis, through the analysis of differential expression genes using the TCGA and GTEx database. A decrease in CD300A expression could promote apoptosis and inhibit proliferation and migration of AML cell line U937, as well as promote the activation of the AKT/mTOR pathway. These results demonstrated that CD300A operated as a tumor promoter in AML cells. We further analyzed coexpression genes of CD300A and then screened two genes, ADCY7 and PECAM1, which were both overexpressed and associated with poor prognosis in AML. Meanwhile, CD300A increased the expression of PECAM1 and ADCY7 in U937 cells. Furthermore, we demonstrated that PECAM1 promoted the proliferation and migration and inhibited the apoptosis of U937 cells. ADCY7 participated in the regulation of proliferation and migration, but not apoptosis, in U937 cells. Both PECAM1 and ADCY7 promoted tumor progression through the AKT pathway, showing the same molecular mechanism as CD300A. To summarize, we, for the first time, confirmed that CD300A promoted tumor progression by increase PECAM1 and ADCY7 expression, and activating the AKT/mTOR signaling pathway in AML. It is suggested CD300A is an oncogene and potential therapeutic target for AML.