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Romo1 is associated with ROS production and cellular growth in human gliomas

Authors
Yu, Mi OkSong, Na-HyunPark, Kyung-JaePark, Dong-HyukKim, Se-HyukChae, Yang-SeokChung, Yong-GuChi, Sung-GilKang, Shin-Hyuk
Issue Date
Jan-2015
Publisher
SPRINGER
Keywords
Romo1; Reactive oxygen species; Tumorigenicity; Glioma
Citation
JOURNAL OF NEURO-ONCOLOGY, v.121, no.1, pp.73 - 81
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF NEURO-ONCOLOGY
Volume
121
Number
1
Start Page
73
End Page
81
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/94879
DOI
10.1007/s11060-014-1608-x
ISSN
0167-594X
Abstract
Romo1 is a mitochondrial protein whose elevated expression is commonly observed in various types of human cancers. However, the expression status of Romo1 and its implication in the pathogenesis of human glioblastoma (GBM) remain largely undefined. To understand the role of Romo1 in the progression of GBM, we explored its expression in a series of GBM tissues and cell lines and determined its effect on ROS production, cell proliferation, and tumor growth. Romo1 was frequently overexpressed at the mRNA level in both primary tumors and cell lines and its elevation was more commonly observed in high grade tumors versus low grade tumors. Romo1 expression was associated with ROS production and its knockdown led to a marked reduction of in vitro cellular growth and anchor-age-independent growth of GBM. Consistently, Romo1 depletion induced a G2/M arrest of the cell cycle that was accompanied with accumulation of phospho-cdc2. Furthermore, a mouse xenograft assay revealed that Romo1 depletion significantly decreased tumor formation and growth. Therefore, our data demonstrate that Romo1 upregulation is a common event in human GBMs and contributes to the malignant tumor progression, suggesting that Romo1 could be a new therapeutic target for human GBM.
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