SLAMF1 contributes to cell survival through the AKT signaling pathway in Farage cells

SLAMF1 is often overexpressed in Epstein Barr virus (EBV)-infected B cell tumors. However, its role in the pathogenesis of EBV-infected B cell tumors remains largely unknown. Here, we generated SLAMF1-deficient EBV+ tumor cells and examined the effect of its deficiency on cell proliferation and cell...

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Bibliographic Details
Published in:PloS one 2020-09, Vol.15 (9), p.e0238791-e0238791
Main Authors: Yoon, Heejei, Kim, Eung Kweon, Ko, Young Hyeh
Format: Article
Language:English
Subjects:
AKT protein
Antibodies
Apoptosis
BIM protein
Biology and Life Sciences
Biotechnology
Cell cycle
Cell growth
Cell proliferation
Cell survival
Cellular signal transduction
Cloning
CRISPR
Epstein-Barr virus
Gene mutation
Genetic aspects
Growth factors
Health aspects
Laboratories
Lymphoma
Medicine
Medicine and Health Sciences
Mutation
Nutrition
Nutritional status
Pathogenesis
Research and Analysis Methods
Signal transduction
Survival
Survival factor
Tumor cells
Tumors
Viruses
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Summary:SLAMF1 is often overexpressed in Epstein Barr virus (EBV)-infected B cell tumors. However, its role in the pathogenesis of EBV-infected B cell tumors remains largely unknown. Here, we generated SLAMF1-deficient EBV+ tumor cells and examined the effect of its deficiency on cell proliferation and cell survival. There were no significant differences in cell proliferation and cell cycle distribution for short periods between the SLAMF1-deficient and wild-type cells. However, the deficient cells were more resistant to an AKT inhibitor (MK-2206). When the both cells were co-cultured and repeatedly exposed to the limitations in nutrition and growth factors, the SLAMF1-deficient cells were gradually decreased. We observed that levels of phospho-AKT were differentially regulated according to the nutritional status between the SLAMF1-deficient and wild-type cells. A decrease in phospho-AKT was observed in SLAMF1-deficient cells as well as an increase in pro-apoptotic Bim just before cell passage, which may have been due to the loss of SLAMF1 under poor growth condition. Overall, SLAMF1 is not a strong survival factor, but it seems to be necessary for cell survival in unfavorable growth condition.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0238791