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Title 

Prx I suppresses K-ras-driven lung tumorigenesis by opposing redox-sensitive ERK/cyclin D1 pathway

Authors 

Young Ho ParkSun-Uk KimBo Kyoung LeeH S KimI S SongHye Jun ShinY H HanKyu Tae ChangJ M KimD S LeeY H KimC M ChoiBo Yeon KimDae Yeul Yu

Publisher 

Mary Ann Liebert

Issue Date 

2013

Citation 

Antioxidants and Redox Signaling, vol. 19, no. 5, pp. 482-496

Abstract 

Aims: Coupled responses of mutated K-ras and oxidative stress are often an important etiological factor in non-small-cell lung cancer (NSCLC). However, relatively few studies have examined the control mechanism of oxidative stress in oncogenic K-ras-driven NSCLC progression. Here, we studied whether the redox signaling pathway governed by peroxiredoxin I (Prx I) is involved in K-ras G12D-mediated lung adenocarcinogenesis. Results: Using human-lung adenocarcinoma tissues and lung-specific K-rasG12D-transgenic mice, we found that Prx I was significantly up-regulated in the tumor regions via activation of nuclear erythroid 2-related factor 2 (Nrf2) transcription. Interestingly, the increased reactive oxygen species (ROS) by null mutation of Prx I greatly promoted K-rasG12D-driven lung tumorigenesis in number and size, which appeared to require the activation of the ROS-dependent extracellular signal-regulated kinase (ERK)/cyclin D1 pathway. Innovation: Taken together, these results suggest that Prx I functions as an Nrf2-dependently inducible tumor suppressant in K-ras-driven lung adenocarcinogenesis by opposing ROS/ERK/cyclin D1 pathway activation. Conclusion: These findings provide a better understanding of oxidative stress-mediated lung tumorigenesis.

ISSN 

1523-0864

Link 

http://dx.doi.org/10.1089/ars.2011.4421

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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