Peroxiredoxin1, a novel regulator of pronephros development, influences retinoic acid and Wnt signaling by controlling ROS levels

Chae, Soomin; Lee, Hyun-Kyung; Kim, Yoo-Kyung; Sim, Hyo Jung; Ji, Yoorim; Kim, Chowon; Ismail, Tayaba; Park, Jeen‐Woo; Kwon, Oh Nam; Kang, Beom-Sik; Lee, Dong‐Seok; Bae, Jong‐Sup; Kim, Sang-Hyun; Min, Kyoung‐jin; Kwon, Taeg Kyu; Park, Mae-Ja; Han, Jin‐Kwan; Kwon, Taejoon; Park, Tae-Joo; Lee, Hyun‐Shik

doi:10.1038/s41598-017-09262-6

Cited by 21 publications

(13 citation statements)

References 45 publications

(55 reference statements)

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“…However, multiple mechanisms have been proposed to explain Prdx1's effects on cilia depolymerization. Chae Soomin et al(44) found that Prdx1 knockdown markedly inhibited proximal tubule formation in the pronephros during embryogenesis, significantly increased the cellular levels of reactive oxygen species (ROS), and impaired primary cilia formation, findings that do not agree with our observations. The difference in activities may reflect different roles of Prdx1 in cilia formation for different cellular components and different disease conditions.…”

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confidence: 99%

Prdx1 Promotes the Loss of Primary Cilia in Esophageal Squamous Cell Carcinoma

Chen

Yang

et al. 2020

Preprint

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Background: Loss of primary cilia is frequently observed in tumor cells, suggesting that the absence of this organelle may promote tumorigenesis through aberrant signal transduction, the inability to exit the cell cycle, and promotion of tumor cell invasion. Primary cilia loss also occurs in esophageal squamous cell carcinoma (ESCC) cells, but the molecular mechanisms that explain how ESCC cells lose primary cilia remain poorly understood. Methods: Inhibiting the expression of Prdx1 in the ESCC cells to detect the up-regulated genes related to cilium regeneration and down-regulated genes related to cilium disassembly by Gene chip. And, mice and cell experiments were carried to confirm the role of the HEF1-Aurora A-HDAC6 signaling axis in ESCC. Results: In this study, we found that silencing Peroxiredoxin 1 (Prdx1) restores primary cilia formation, and over-expressing Prdx1 induces primary cilia loss in ESCC cells. We also showed that the expression of Prdx1 regulates the action of the HEF1-Aurora A-HDAC6 signaling axis to promote the disassembly of primary cilia, and suppression of Prdx1 results in decreased tumor formation and tumor mass volume in vivo. Conclusions: These results suggest that Prdx1 is a novel regulator of primary cilia formation in ESCC cells.

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confidence: 99%

Prdx1 Promotes the Loss of Primary Cilia in Esophageal Squamous Cell Carcinoma

Chen

Yang

et al. 2020

Preprint

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“…However, multiple mechanisms have been proposed to explain Prdx1's effects on cilia depolymerization. Chae Soomin et al [44] found that Prdx1 knockdown (See figure on previous page.) Fig.…”

Section: Discussionmentioning

confidence: 99%

Prdx1 promotes the loss of primary cilia in esophageal squamous cell carcinoma

Chen

Yang

et al. 2020

BMC Cancer

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Background: Loss of primary cilia is frequently observed in tumor cells, suggesting that the absence of this organelle may promote tumorigenesis through aberrant signal transduction, the inability to exit the cell cycle, and promotion of tumor cell invasion. Primary cilia loss also occurs in esophageal squamous cell carcinoma (ESCC) cells, but the molecular mechanisms that explain how ESCC cells lose primary cilia remain poorly understood. Methods: Inhibiting the expression of Prdx1 in the ESCC cells to detect the up-regulated genes related to cilium regeneration and down-regulated genes related to cilium disassembly by Gene chip. And, mice and cell experiments were carried to confirm the role of the HEF1-Aurora A-HDAC6 signaling axis in ESCC. Results: In this study, we found that silencing Peroxiredoxin 1 (Prdx1) restores primary cilia formation, and overexpressing Prdx1 induces primary cilia loss in ESCC cells. We also showed that the expression of Prdx1 regulates the action of the HEF1-Aurora A-HDAC6 signaling axis to promote the disassembly of primary cilia, and suppression of Prdx1 results in decreased tumor formation and tumor mass volume in vivo. Conclusions: These results suggest that Prdx1 is a novel regulator of primary cilia formation in ESCC cells.

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“…Prdxs denote the family of proteins having the ability to efficiently scavenge peroxides in the form of hydrogen peroxide, alkyl hydro peroxide, and peroxynitrite [33]. Prdxs are classified into six subfamilies, according to PeroxiRedoxin classification index (PREX) and, in mammals, there are six Prdxs, among which Prdx 1–4 belongs to Prdx1 subfamily, Prdx5 is a member of Prdx5 subfamily, and Prdx6 represent Prdx6 subfamily [34,35]. Prdxs are also classified as 1-Cys containing only Prdx6, while typical 2-Cys comprised of Prdx1–4 and Prdx5 belongs to atypical 2-Cys on the basis of their cysteine residues and their catalytic mechanism [36].…”

Section: Mitochondrial Prdxsmentioning

confidence: 99%

“…Both mitochondrial Prdxs comprise peroxidatic cysteine (Cp) and resolving cysteine (Cr) which play an essential role in their catalytic mechanisms. In Prdx3, Cp is located at residue 47, whereas, in Prdx5, it is located at residue 48 [35].…”

Section: Figurementioning

confidence: 99%

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

Ismail

Kim

Lee

et al. 2019

IJMS

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102

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Mitochondria are multifunctional cellular organelles that are major producers of reactive oxygen species (ROS) in eukaryotes; to maintain the redox balance, they are supplemented with different ROS scavengers, including mitochondrial peroxiredoxins (Prdxs). Mitochondrial Prdxs have physiological and pathological significance and are associated with the initiation and progression of various cancer types. In this review, we have focused on signaling involving ROS and mitochondrial Prdxs that is associated with cancer development and progression. An upregulated expression of Prdx3 and Prdx5 has been reported in different cancer types, such as breast, ovarian, endometrial, and lung cancers, as well as in Hodgkin’s lymphoma and hepatocellular carcinoma. The expression of Prdx3 and Prdx5 in different types of malignancies involves their association with different factors, such as transcription factors, micro RNAs, tumor suppressors, response elements, and oncogenic genes. The microenvironment of mitochondrial Prdxs plays an important role in cancer development, as cancerous cells are equipped with a high level of antioxidants to overcome excessive ROS production. However, an increased production of Prdx3 and Prdx5 is associated with the development of chemoresistance in certain types of cancers and it leads to further complications in cancer treatment. Understanding the interplay between mitochondrial Prdxs and ROS in carcinogenesis can be useful in the development of anticancer drugs with better proficiency and decreased resistance. However, more targeted studies are required for exploring the tumor microenvironment in association with mitochondrial Prdxs to improve the existing cancer therapies and drug development.

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Peroxiredoxin1, a novel regulator of pronephros development, influences retinoic acid and Wnt signaling by controlling ROS levels

Cited by 21 publications

References 45 publications

Prdx1 Promotes the Loss of Primary Cilia in Esophageal Squamous Cell Carcinoma

Prdx1 Promotes the Loss of Primary Cilia in Esophageal Squamous Cell Carcinoma

Prdx1 promotes the loss of primary cilia in esophageal squamous cell carcinoma

Interplay Between Mitochondrial Peroxiredoxins and ROS in Cancer Development and Progression

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