دورية أكاديمية
أعرض في EDS

Arylamine N-acetyltransferase 1 deficiency inhibits drug-induced cell death in breast cancer cells: switch from cytochrome C-dependent apoptosis to necroptosis.

التفاصيل البيبلوغرافية
العنوان: Arylamine N-acetyltransferase 1 deficiency inhibits drug-induced cell death in breast cancer cells: switch from cytochrome C-dependent apoptosis to necroptosis.
المؤلفون: McAleese CE; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, 4072, Australia., Butcher NJ; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, 4072, Australia., Minchin RF; School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, 4072, Australia. r.minchin@uq.edu.au.
المصدر: Breast cancer research and treatment [Breast Cancer Res Treat] 2022 Oct; Vol. 195 (3), pp. 223-236. Date of Electronic Publication: 2022 Aug 02.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Kluwer Academic Country of Publication: Netherlands NLM ID: 8111104 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-7217 (Electronic) Linking ISSN: 01676806 NLM ISO Abbreviation: Breast Cancer Res Treat Subsets: MEDLINE
أسماء مطبوعة: Publication: Dordrecht : Kluwer Academic
Original Publication: The Hague ; Boston : M. Nijhoff, c1981-
مواضيع طبية MeSH: Antineoplastic Agents*/pharmacology , Antineoplastic Agents*/therapeutic use , Arylamine N-Acetyltransferase*/deficiency , Arylamine N-Acetyltransferase*/genetics , Breast Neoplasms*/drug therapy , Breast Neoplasms*/genetics , Breast Neoplasms*/metabolism, Apoptosis ; Caspase 8/genetics ; Caspase 8/metabolism ; Caspase 8/therapeutic use ; Cell Death ; Cytochromes c/metabolism ; Cytochromes c/therapeutic use ; Female ; Humans ; Isoenzymes/deficiency ; Isoenzymes/genetics ; Necroptosis
مستخلص: Purpose: Arylamine N-acetyltransferase 1 (NAT1) deficiency has been associated with drug resistance and poor outcomes in breast cancer patients. The current study aimed to investigate drug resistance in vitro using normal breast cancer cell lines and NAT1-deficient cell lines to understand the changes induced by the lack of NAT1 that resulted in poor drug response.
Methods: The response to seven chemotherapeutic agents was quantified following NAT1 deletion using CRISPR-Cas 9 in MDA-MB-231 and T-47D cells. Apoptosis was monitored by annexin V staining and caspase 3/7 activity. Cytochrome C release and caspase 8 and 9 activities were measured by Western blots. Caspase 8 was inhibited using Z-IETD-FMK and necroptosis was inhibited using necrostatin and necrosulfonamide.
Results: Compared to parental cells, NAT1 depleted cells were resistant to drug treatment. This could be reversed following NAT1 rescue of the NAT1 deleted cells. Release of cytochrome C in response to treatment was decreased in the NAT1 depleted cells, suggesting suppression of the intrinsic apoptotic pathway. In addition, NAT1 knockout resulted in a decrease in caspase 8 activation. Treatment with necrosulfonamide showed that NAT1 deficient cells switched from intrinsic apoptosis to necroptosis when treated with the anti-cancer drug cisplatin.
Conclusions: NAT1 deficiency can switch cell death from apoptosis to necroptosis resulting in decreased response to cytotoxic drugs. The absence of NAT1 in patient tumours may be a useful biomarker for selecting alternative treatments in a subset of breast cancer patients.
(© 2022. The Author(s).)
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معلومات مُعتمدة: 1083036 National Health and Medical Research Council
فهرسة مساهمة: Keywords: Apoptosis; Breast cancer; Drug resistance; NAT1; Necroptosis
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Isoenzymes)
9007-43-6 (Cytochromes c)
EC 2.3.1.5 (Arylamine N-Acetyltransferase)
EC 2.3.1.5 (N-acetyltransferase 1)
EC 3.4.22.- (Caspase 8)
تواريخ الأحداث: Date Created: 20220802 Date Completed: 20220913 Latest Revision: 20220922
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9464750
DOI: 10.1007/s10549-022-06668-3
PMID: 35918499
قاعدة البيانات: MEDLINE
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