Please use this identifier to cite or link to this item: http://cuir.car.chula.ac.th/handle/123456789/62129
Title: LINE-1 ORF1 Protein Is Up-regulated by Reactive Oxygen Species and Associated with Bladder Urothelial Carcinoma Progression
Authors: PATCHARAWALAI WHONGSIRI
DEPICHA JINDATIP
ANAPAT SANPAVAT
Email: Depicha.J@chula.ac.th
Anapat.S@Chula.ac.th
Other author: Chulalongkorn University. Faculty of Medicine
Issue Date: Mar-2018
Publisher: International Institute of Anticancer Research
Citation: Cancer Genomics and Proteomics March-April 2018 vol. 15 no. 2 p.143-151
Abstract: Background/Aim: Reactivation of long interspersed nuclear element-1 (LINE-1) and oxidative stress are suggested to have oncogenic potential to drive tumorigenesis and cancer progression. We previously demonstrated that reactive oxygen species (ROS) caused hypomethylation of LINE-1 elements in bladder cancer cells. In this study, we investigated the expression of LINE-1-encoded protein (ORF1p) and oxidative stress marker 4-hydroxynonenal (4-HNE) in human bladder cancer tissues, as well as induction of ORF1p expression by ROS in bladder cancer cell lines. Materials and Methods: Thirty-six cancerous and 15 non-cancerous adjacent tissues were immunohistochemically stained for ORF1p and 4-HNE. ORF1p expression and cell migration were determined in bladder cancer cells exposed to H2O2. Results: ORF1p and 4-HNE expression was higher in cancerous than non-cancerous tissues. Elevated ORF1p expression was associated with increased 4-HNE expression and with advanced tumors. H2O2 provoked oxidative stress and up-regulated ORF1p expression in VM-CUB-1 compared to the untreated control, and to a lesser degree in TCCSUP. H2O2 exposure enhanced cell migration in UM-UC-3, TCCSUP and VM-CUB-1. Conclusion: Elevated ORF1p expression is associated with tumor progression. ROS experimentally induce ORF1p expression and promote migration in bladder cancer cells.
URI: http://cuir.car.chula.ac.th/handle/123456789/62129
URI: http://doi.org/10.21873/cgp.20072
http://cgp.iiarjournals.org/content/15/2/143
ISSN: 1109-6535
metadata.dc.identifier.DOI: 10.21873/cgp.20072
Type: Article
Appears in Collections:Chula Scholars - 2018

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