Peroxiredoxin 1 regulates crosstalk between pyroptosis and autophagy in oral squamous cell carcinoma leading to a potential pro-survival.
Journal
Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035
Informations de publication
Date de publication:
25 Nov 2023
25 Nov 2023
Historique:
received:
08
05
2023
accepted:
13
11
2023
revised:
24
10
2023
medline:
26
11
2023
pubmed:
26
11
2023
entrez:
25
11
2023
Statut:
epublish
Résumé
Peroxiredoxin 1 (Prdx1), a vital antioxidant enzyme, has been proven to play an important role in the occurrence and development of cancers, but its effects on oral squamous cell carcinoma (OSCC) remain unclear. Here, we performed bioinformatics analysis and immunohistochemical (IHC) staining to confirm that Prdx1 was higher in OSCC tissues than in normal tissues. Consistently, RT-PCR and Western blot showed elevated Prdx1 expression in OSCC cell lines compared to human oral keratinocytes (HOK), which could be knockdown by small interfering RNA (siRNA) and Lentiviral vector delivery of short hairpin RNA (shRNA). Prdx1 silencing significantly blocked OSCC cell proliferation and metastasis, as evidenced by the CCK8, colony formation, in vivo tumorigenesis experiment, wound healing, transwell assays, and changes in migration-related factors. siPrdx1 transfection increased intracellular reactive oxygen species (ROS) levels and provoked pyroptosis, proved by the upregulation of pyroptotic factors and LDH release. Prdx1 silencing ROS-independently blocked autophagy. Mature autophagosome failed to form in the siPrdx1 group. Up-regulated autophagy limited pyroptosis triggered by Prdx1 deficiency, and down-regulated pyroptosis partly reversed siPrdx1-induced autophagy defect. Collectively, Prdx1 regulated pyroptosis in a ROS-dependent way and modulated autophagy in a ROS-independent way, involving the crosstalk between pyroptosis and autophagy.
Identifiants
pubmed: 38007535
doi: 10.1038/s41420-023-01720-7
pii: 10.1038/s41420-023-01720-7
pmc: PMC10676359
doi:
Types de publication
Journal Article
Langues
eng
Pagination
425Subventions
Organisme : National Natural Science Foundation of China (National Science Foundation of China)
ID : (No. 81800982
Organisme : National Natural Science Foundation of China (National Science Foundation of China)
ID : No. 81972072
Organisme : Taishan Scholar Foundation of Shandong Province
ID : No. tstp20221160
Informations de copyright
© 2023. The Author(s).
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