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

Authors
 Heejei Yoon  ;  Eung Kweon Kim  ;  Young Hyeh Ko 
Citation
 PLOS ONE, Vol.15(9) : e0238791, 2020-09 
Journal Title
 PLOS ONE 
Issue Date
2020-09
MeSH
B-Lymphocytes / metabolism ; Cell Survival ; Herpesvirus 4, Human / metabolism ; Humans ; Proto-Oncogene Proteins c-akt / metabolism* ; Signal Transduction ; Signaling Lymphocytic Activation Molecule Family Member 1 / metabolism* ; Tumor Cells, Cultured
Abstract
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.
Files in This Item:
T202004596.pdf Download
DOI
10.1371/journal.pone.0238791
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Eung Kweon(김응권) ORCID logo https://orcid.org/0000-0002-1453-8042
Yoon, Heejei(윤희제)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/180324
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