Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway
Authors Song Y, Liu H, Cui C, Peng X, Wang C, Tian X, Li W
Received 19 October 2019
Accepted for publication 12 December 2019
Published 30 December 2019 Volume 2019:11 Pages 10883—10890
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Beicheng Sun
Yingjian Song,1,* Huimin Liu,2,* Chunling Cui,3 Xiaonu Peng,1 Chaoyang Wang,1 Xudong Tian,4 Wenjun Li1
1Department of Thoracic Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, Shandong, People’s Republic of China; 2Department of Gastroenterology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, Shandong, People’s Republic of China; 3Library, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, Shandong, People’s Republic of China; 4Department of Thoracic Surgery, Liaocheng People’s Hospital, Liaocheng 252000, Shandong, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xudong Tian
Department of Thoracic Surgery, Liaocheng People’s Hospital, No. 67, Changxi Road, Liaocheng, Shandong 252000, People’s Republic of China
Department of Thoracic Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, No. 20 Yuhungding East Road, Zhifu District, Yantai 264000, Shandong, People’s Republic of China
Objective: To 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.
Methods: Three 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.
Results: The 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.
Conclusion: PRDX1 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.
Keywords: peroxiredoxin 1, esophageal squamous cell carcinoma, PI3K/AKT signaling pathway, proliferation, apoptosis
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]