ArticleCancer management and research2019
Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Conditional knockout mouse model reveals a critical role of peroxiredoxin 1 in oral leukoplakia carcinogenesis.Heliyon · 2024Article
- NEK2 promotes the migration, invasion, proliferation of ESCC and mediates ESCC immunotherapy.Heliyon · 2024Article
- Carcinogenic Role and Clinical Significance of Histone H3-H4 Chaperone Anti-silencing Function 1 B (ASF1B) in Lung Adenocarcinoma.Journal of Cancer · 2024Article
- Peroxiredoxin 1 regulates crosstalk between pyroptosis and autophagy in oral squamous cell carcinoma leading to a potential pro-survival.Cell death discovery · 2023Article
- Expression And Prognostic Role of PRDX1 In Gastrointestinal Cancers.Journal of Cancer · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- The beginning of GPX2 and 30 years later.Free radical biology & medicine · 2022Review
- Knockdown of DEAD-box 51 inhibits tumor growth of esophageal squamous cell carcinomaWorld journal of gastroenterology · 2022Article
- Using network pharmacology approaches to identify treatment mechanisms for codonopsis in esophageal cancer.International journal of clinical and experimental pathology · 2022Article
- Zearalenone promotes apoptosis of mouse Leydig cells by targeting phosphatase and tensin homolog and thus inhibiting the PI3K/AKT signal pathway.Environmental science and pollution research international · 2021Article
- miR-15b, a diagnostic biomarker and therapeutic target, inhibits oesophageal cancer progression by regulating the PI3K/AKT signalling pathway.Experimental and therapeutic medicine · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo study the effect of peroxiredoxin 1 (PRDX1) on esophageal squamous carcinoma cells and determine whether it plays a role in regulating the PI3K/AKT signaling pathway.
methodsThree esophageal squamous cell carcinoma cell lines (Eca-109, EC9706, and KYSE150) and one normal cell line (human esophageal epithelial cells) were selected. The protein expression of peroxiredoxin 1 (PRDX1) and the activity of the PI3K/AKT pathway were detected via Western blotting. The proliferation ability of cells was detected through the MTT assay and cell clone formation. Apoptosis was detected using flow cytometry. Subsequently, cells were treated with a PI3K/AKT pathway inhibitor and activator, alone or in combination with silencing of PRDX1, and the above indicators were re-tested.
resultsThe expression of PRDX1 and activity of PI3K/AKT pathway-associated proteins were higher in esophageal cancer cells than in normal esophageal epithelial cells. Compared with normal human esophageal epithelial cells, the proliferation of the three types of esophageal cancer cells was increased, whereas their level of apoptosis was decreased (p<0.05). In Eca-109 cells (cell line with silenced expression of PRDX1), the expression of PRDX1 was significantly decreased. In contrast to the control group, the proliferation and clonality of cells in the silencing PRDX1 group was decreased, the proportion of apoptotic cells was increased, and the phosphorylation levels of PI3K and AKT were decreased (p<0.05). Compared with the control group, treatment with the inhibitor LY294002 alone significantly inhibited cell proliferation and promoted apoptosis (p<0.05); this effect was similar to that observed in the silencing PRDX1 group.
conclusionPRDX1 was highly expressed in esophageal cancer cells. Silencing of PRDX1 can inhibit the proliferation of esophageal cancer cells and promote apoptosis. The mechanism involved in this process may be related to the inhibition of the PI3K/AKT signaling pathway.
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