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Int J Oncol. 2016 Oct;49(4):1469-78. doi: 10.3892/ijo.2016.3623. Epub 2016 Jul 15.

Metabotropic glutamate receptor 3 is involved in B-cell-related tumor apoptosis.

Author information

1
Laboratory of Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
2
College of Pharmacy, Henan University, Kaifeng, Henan 475001, P.R. China.
3
Department of Rheumatology, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract

Cell apoptosis plays a critical role in initiation and progression of tumor and autoimmune diseases, resistance and susceptibility to various therapeutic agents. Our previous study showed that metabotropic glutamate receptor 3 (Grm3) may be involved in autoreactive B-cell apoptosis in a B-cell-depleted agent atacicept-treated lupus-like mice. In the present study, we explore whether Grm3 is involved in the apoptosis in B-cell-related tumor including multiple myeloma and B-cell leukemia. We found that human B-cell leukemia cell line Nalm-6 cells and mouse myeloma cell line SP 2/0 cells could express Grm3. In addition, Grm3 expression emerged mainly in the middle stage of Nalm-6 and SP 2/0 cell apoptosis. Furthermore, apoptosis-induced agents effectively upregulated Grm3 expression in SP 2/0 cells. Critically, Grm3 deficiency promoted tumor progression in an SP 2/0 xenograft mouse model by suppressing cell apoptosis, whereas Grm3 overexpression effectively upregulates SP 2/0 cell apoptosis. Finally, we showed that Grm3 mediated cell apoptosis by Foxo1. Together, our data suggest that Grm3 effectively suppresses the mouse myeloma cell line SP 2/0 cell growth by mediating apoptosis. Thus, Grm3 may be used as an indicator in apoptosis of B-cell-related tumor and a potential target for the treatment of B-cell-related tumor including multiple myeloma and B-cell leukemia.

PMID:
27431857
DOI:
10.3892/ijo.2016.3623
[Indexed for MEDLINE]

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