ArticleBioMed research international2020
Silencing of PRDX2 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer Cells.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Knockdown of PRDX2 Inhibits the Proliferation, Growth, Migration, Invasion, and MMP9 Activity of Ewing's Sarcoma Cells Cultured In Vitro.Cancer reports (Hoboken, N.J.) · 2024Article
- The Role of Peroxiredoxins in Cancer Development.Biology · 2023Review
- Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma.Oncology research · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- MnTnHex-2-PyPAntioxidants (Basel, Switzerland) · 2022Article
- Endoplasmic Reticulum Stress and Impairment of Ribosome Biogenesis Mediate the Apoptosis Induced byMedicina (Kaunas, Lithuania) · 2022Article
- PRDX2 Promotes the Proliferation and Metastasis of Non-Small Cell Lung CancerBioMed research international · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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