Silencing of PRDX2 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer Cells.
Journal
BioMed research international
ISSN: 2314-6141
Titre abrégé: Biomed Res Int
Pays: United States
ID NLM: 101600173
Informations de publication
Date de publication:
2020
2020
Historique:
received:
04
11
2019
revised:
24
02
2020
accepted:
25
02
2020
entrez:
28
4
2020
pubmed:
28
4
2020
medline:
30
1
2021
Statut:
epublish
Résumé
Peroxiredoxin 2 (PRDX2), a member of the peroxiredoxin family of antioxidant enzymes, has been revealed to be an important player in cancer progression. However, the biological role of PRDX2 in the progression of non-small cell lung cancer (NSCLC) is poor reported. In the present study, the loss-of-function experiments were performed to investigate the specific role of PRDX2 in the growth and invasion of NSCLC. The results revealed that knockdown of PRDX2 by siRNA interference significantly suppressed the proliferation, migration, and invasion of A549 and H1299 cells, as well as diminished the activity of MMP9. Additionally, the decrease in PRDX2 expression significantly promoted apoptosis in NSCLC cells by downregulating expression of Bcl-2 and upregulating the expression of Bax, cleaved caspase 3 and cleaved caspase 9, but had no significant effect on the apoptosis of normal lung epithelial cells BEAS-2B. Moreover, PRDX2 inhibitor also inhibited the proliferation, migration, and invasion of A549 cells and promoted apoptosis. Further, our data demonstrated that silencing of PRDX2 markedly reduced the phosphorylation of Akt and mTOR and expression of downstream proteins Cyclin D1 and p70S6k. In conclusion, our findings indicate that PRDX2 exerts a prooncogenic role in the progression of NSCLC and might be a potential therapeutic target for NSCLC treatment.
Identifiants
pubmed: 32337219
doi: 10.1155/2020/1276328
pmc: PMC7157786
doi:
Substances chimiques
PRDX2 protein, human
EC 1.11.1.15
Peroxiredoxins
EC 1.11.1.15
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1276328Informations de copyright
Copyright © 2020 Xu Jing et al.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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