Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P42345 (
mTOR
)
26,049
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID:CD300A promotes tumor progression by PECAM1, ADCY7 and AKT pathway in acute myeloid leukemia. 2993 7