Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P31749 (AKT)
 22,954 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD300A is a type I transmembrane receptor protein which has shown inhibitory effects on B-cell receptor-mediated signals. In an analysis of public dataset, we found that CD300A mRNA levels were inversely correlated with the overall survival time of patients with diffuse large B-cell lymphoma (DLBCL). To decipher the role of CD300A in DLBCL, we knocked down the expression levels of CD300A in DLBCL cells and found that decreasing levels of CD300A significantly inhibited cell proliferation of OCI-Ly01, Farage, and SUDHL-4 cells, but not of VAL, OCI-Ly10, or SUDHL-8 cells. Mechanistically, reduced expression of CD300A resulted in a marked attenuation of AKT phosphorylation, a key molecular event in tumorigenesis, in OCI-Ly01, Farage, and SUDHL-4 cells. Pharmacologic inhibition of PI3K displayed a similar inhibitory effect on cell proliferation. Furthermore, using a xenograft animal model, we found that decreasing levels of CD300A in OCI-Ly01 and Farage cells significantly inhibited tumor formation in vivo. Collectively, our results suggested an oncogenic role of CD300A in DLBCL which could serve as a potential biomarker and therapeutic target for this malignant disease.
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PMID:Suppression of CD300A inhibits the growth of diffuse large B-cell lymphoma. 2849 31

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.
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PMID:CD300A promotes tumor progression by PECAM1, ADCY7 and AKT pathway in acute myeloid leukemia. 2993 7

Glioblastoma multiforme (GBM) is a primary malignant tumor of the central nervous system with the highest incidence and dismal prognosis. As a member of the CD300 glycoprotein family, CD300A plays a role in cell proliferation, apoptosis, differentiation, and immune response, but its role in solid tumors remains unknown. In this study, CD300A was observed to be overexpressed in human GBM samples using real-time PCR and western blotting. To investigate the role of CD300A in GBM, CCK8, transwell and flow cytometry analysis were performed to examine the proliferation, migration and apoptosis in GBM cell lines, respectively. From our results, knockdown of CD300A blocks cell proliferation and migration, and induces cell apoptosis in human GBM cells U251MG and U87MG. Further, we assessed AKT expression level in CD300A knockdown and negative control cells. The phosphorylation level of AKT was significantly suppressed in CD300A knockdown cells in comparison to negative control cells, suggesting that CD300A promoted tumor cell growth through the AKT pathway. In conclusion, our findings expand the knowledge of CD300A as an oncogene in solid tumor, and provide experimental and theoretical basis for further clinical application.
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PMID:CD300A inhibits tumor cell growth by downregulating AKT phosphorylation in human glioblastoma multiforme. 3194 25