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Bcl-2 hijacks the arsenic trioxide resistance in SH-SY5Y cells

Wang, Jinling ; Peng, Xiaohui ; Yang, Daowei LU ; Guo, Mengyu ; Xu, Xiao ; Yin, Fengyue ; Wang, Yu ; Huang, Jiaqing ; Zhan, Linghui and Qi, Zhongquan (2022) In Journal of Cellular and Molecular Medicine 26(2). p.563-569
Abstract

Aresenic trioxide (ATO) is proven to be active against leukaemia cells by inducing apoptosis and differentiation. Even though ATO could effectively induce remissions of leukaemia cells, the drug resistance was observed occasionally. To further dissect the mechanism of ATO resistance, we selected the ATO-resistant SH-SY5Y cells and found that Bcl-2 controlled the sensitivity of ATO in SH-SY5Y cells. We report that necroptosis, autophagy, NF-ƘB and MAPK signalling pathway are not involved in ATO-induced apoptosis. Moreover, the ATO-resistant cells showed distinct mitochondrial morphology compared with that of ATO-sensitive cells. Intriguingly, nude mice-bearing ATO-sensitive cells derived xenograft tumours are more sensitive to ATO... (More)

Aresenic trioxide (ATO) is proven to be active against leukaemia cells by inducing apoptosis and differentiation. Even though ATO could effectively induce remissions of leukaemia cells, the drug resistance was observed occasionally. To further dissect the mechanism of ATO resistance, we selected the ATO-resistant SH-SY5Y cells and found that Bcl-2 controlled the sensitivity of ATO in SH-SY5Y cells. We report that necroptosis, autophagy, NF-ƘB and MAPK signalling pathway are not involved in ATO-induced apoptosis. Moreover, the ATO-resistant cells showed distinct mitochondrial morphology compared with that of ATO-sensitive cells. Intriguingly, nude mice-bearing ATO-sensitive cells derived xenograft tumours are more sensitive to ATO treatment compared with that of ATO-resistant cells. These data demonstrate that cancer cells can acquire the ATO-resistance ability by increasing the Bcl-2 expression.

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author
; ; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Cellular and Molecular Medicine
volume
26
issue
2
pages
7 pages
publisher
Wiley-Blackwell
external identifiers
  • pmid:34910369
  • scopus:85121286475
ISSN
1582-1838
DOI
10.1111/jcmm.17128
language
English
LU publication?
yes
id
45b1850a-9c82-4f51-9954-bdd26865c293
date added to LUP
2022-01-31 14:45:47
date last changed
2025-07-30 03:36:00
@article{45b1850a-9c82-4f51-9954-bdd26865c293,
  abstract     = {{<p>Aresenic trioxide (ATO) is proven to be active against leukaemia cells by inducing apoptosis and differentiation. Even though ATO could effectively induce remissions of leukaemia cells, the drug resistance was observed occasionally. To further dissect the mechanism of ATO resistance, we selected the ATO-resistant SH-SY5Y cells and found that Bcl-2 controlled the sensitivity of ATO in SH-SY5Y cells. We report that necroptosis, autophagy, NF-ƘB and MAPK signalling pathway are not involved in ATO-induced apoptosis. Moreover, the ATO-resistant cells showed distinct mitochondrial morphology compared with that of ATO-sensitive cells. Intriguingly, nude mice-bearing ATO-sensitive cells derived xenograft tumours are more sensitive to ATO treatment compared with that of ATO-resistant cells. These data demonstrate that cancer cells can acquire the ATO-resistance ability by increasing the Bcl-2 expression.</p>}},
  author       = {{Wang, Jinling and Peng, Xiaohui and Yang, Daowei and Guo, Mengyu and Xu, Xiao and Yin, Fengyue and Wang, Yu and Huang, Jiaqing and Zhan, Linghui and Qi, Zhongquan}},
  issn         = {{1582-1838}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{563--569}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Journal of Cellular and Molecular Medicine}},
  title        = {{Bcl-2 hijacks the arsenic trioxide resistance in SH-SY5Y cells}},
  url          = {{http://dx.doi.org/10.1111/jcmm.17128}},
  doi          = {{10.1111/jcmm.17128}},
  volume       = {{26}},
  year         = {{2022}},
}