Objectives: Peroxiredoxins (Prxs) are antioxidant enzymes that can coordinate cell signal transduction via reactive species scavenging or by acting as redox sensors. The mechanism by which Prxs promote cancer invasion and progression is not yet fully understood. This study aims to elucidate the precise mechanism through which Prx type 5 (Prx5) promotes cancer invasion and tumor growth. Materials and methods: We analyzed the Prx5 expression in oral squamous cell carcinoma (OSCC) by using microarray analysis for gene expression profiling. To identify Prx5 function in cancer, lentiviral short hairpin RNA was used for Prx5 depletion, and invasion assay and mouse xenograft were performed. Results: In microarray data obtained from OSCC patients, Prx5 showed higher expression at the tumor margin (TM) compared to the tumor center (TC) of the collective invasion. The depletion of Prx5 in OSCC cells (Prx5dep) led to decreased invasion activity. In orthotopic xenograft models, Prx5dep cells harbored delimited tumorigenicity compared to wild-type cells as well as the suppression of lymph node metastasis. Prx5dep cells showed growth retardation and increased cellular reactive oxygen species (ROS) levels. The growth retardation of Prx5dep cells resulted in G1 phase arrest. Conclusions: This study provides evidence that Prx5 removes excess ROS, especially in the TM, contributing to cancer invasion and tumor progression.
|Number of pages||13|
|Publication status||Published - 2023 Mar|
Bibliographical noteFunding Information:
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2018R1D1A1B07042035).
© 2021 Wiley Periodicals LLC.
All Science Journal Classification (ASJC) codes