ArticleJournal of cellular and molecular medicine2022
Bcl-2 hijacks the arsenic trioxide resistance in SH-SY5Y cells.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- ML364 ameliorates NLRP3-induced inflammatory response.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- RGD-decorated nanoliposomes for combined delivery of arsenic trioxide and curcumin to prostate cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The Development and Clinical Applications of Oral Arsenic Trioxide for Acute Promyelocytic Leukaemia and Other Diseases.Pharmaceutics · 2022Review
- Ketamine inhibits TNF-α-induced cecal damage by enhancing RIP1 ubiquitination to attenuate lethal SIRS.Cell death discovery · 2022Article
- Bcl-2 hijacks the arsenic trioxide resistance in SH-SY5Y cells.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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 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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Registered trials
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