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BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma article

Sime, Wondossen LU ; Niu, Qiankun; Abassi, Yasmin LU ; Masoumi, Katarzyna Chmielarska LU ; Zarrizi, Reihaneh LU ; Køhler, Julie Bonne LU ; Kjellström, Sven LU ; Lasorsa, Vito Alessandro; Capasso, Mario and Fu, Haian, et al. (2018) In Cell Death and Disease 9(5).
Abstract

BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that is associated with multiprotein complexes that regulate key cellular pathways, including cell cycle, cellular differentiation, cell death, and the DNA damage response. In this study, we found that the reduced expression of BAP1 pro6motes the survival of neuroblastoma cells, and restoring the levels of BAP1 in these cells facilitated a delay in S and G2/M phase of the cell cycle, as well as cell apoptosis. The mechanism that BAP1 induces cell death is mediated via an interaction with 14-3-3 protein. The association between BAP1 and 14-3-3 protein releases the apoptotic inducer protein Bax from 14-3-3 and promotes cell death through the intrinsic apoptosis... (More)

BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that is associated with multiprotein complexes that regulate key cellular pathways, including cell cycle, cellular differentiation, cell death, and the DNA damage response. In this study, we found that the reduced expression of BAP1 pro6motes the survival of neuroblastoma cells, and restoring the levels of BAP1 in these cells facilitated a delay in S and G2/M phase of the cell cycle, as well as cell apoptosis. The mechanism that BAP1 induces cell death is mediated via an interaction with 14-3-3 protein. The association between BAP1 and 14-3-3 protein releases the apoptotic inducer protein Bax from 14-3-3 and promotes cell death through the intrinsic apoptosis pathway. Xenograft studies confirmed that the expression of BAP1 reduces tumor growth and progression in vivo by lowering the levels of pro-survival factors such as Bcl-2, which in turn diminish the survival potential of the tumor cells. Patient data analyses confirmed the finding that the high-BAP1 mRNA expression correlates with a better clinical outcome. In summary, our study uncovers a new mechanism for BAP1 in the regulation of cell apoptosis in neuroblastoma cells.

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Cell Death and Disease
volume
9
issue
5
publisher
Nature Publishing Group
external identifiers
  • scopus:85045947649
ISSN
2041-4889
DOI
10.1038/s41419-018-0500-6
language
English
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yes
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f75ca2cc-04b3-4685-a2cc-bffd761af957
date added to LUP
2018-05-07 13:01:17
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2019-04-21 05:14:06
@article{f75ca2cc-04b3-4685-a2cc-bffd761af957,
  abstract     = {<p>BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that is associated with multiprotein complexes that regulate key cellular pathways, including cell cycle, cellular differentiation, cell death, and the DNA damage response. In this study, we found that the reduced expression of BAP1 pro6motes the survival of neuroblastoma cells, and restoring the levels of BAP1 in these cells facilitated a delay in S and G2/M phase of the cell cycle, as well as cell apoptosis. The mechanism that BAP1 induces cell death is mediated via an interaction with 14-3-3 protein. The association between BAP1 and 14-3-3 protein releases the apoptotic inducer protein Bax from 14-3-3 and promotes cell death through the intrinsic apoptosis pathway. Xenograft studies confirmed that the expression of BAP1 reduces tumor growth and progression in vivo by lowering the levels of pro-survival factors such as Bcl-2, which in turn diminish the survival potential of the tumor cells. Patient data analyses confirmed the finding that the high-BAP1 mRNA expression correlates with a better clinical outcome. In summary, our study uncovers a new mechanism for BAP1 in the regulation of cell apoptosis in neuroblastoma cells.</p>},
  articleno    = {458},
  author       = {Sime, Wondossen and Niu, Qiankun and Abassi, Yasmin and Masoumi, Katarzyna Chmielarska and Zarrizi, Reihaneh and Køhler, Julie Bonne and Kjellström, Sven and Lasorsa, Vito Alessandro and Capasso, Mario and Fu, Haian and Massoumi, Ramin},
  issn         = {2041-4889},
  language     = {eng},
  month        = {01},
  number       = {5},
  publisher    = {Nature Publishing Group},
  series       = {Cell Death and Disease},
  title        = {BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma article},
  url          = {http://dx.doi.org/10.1038/s41419-018-0500-6},
  volume       = {9},
  year         = {2018},
}