Suppression of CD300A inhibits the growth of diffuse large B-cell lymphoma
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Lei Jiang1, Yulian Xu1, Xinli Zeng2, Jianchen Fang3, Herbert C. Morse III4, Jeff X. Zhou1
1Department of Pathology, Zhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, China
2Department of ENT, Ningbo Second People's Hospital, Ningbo, China
3Ningbo Pathology Service Center, Ningbo, China
4Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA
Jeff X. Zhou, e-mail: firstname.lastname@example.org
Keywords: diffuse large B-cell lymphoma, CD300A, PI3K/AKT, lymphomagenesis
Received: February 23, 2015 Accepted: August 20, 2015 Published: September 02, 2015
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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