@article{523bbd9d87da4b62b716748884e62b53,
title = "Identification of UHRF2 as a Negative Regulator of Epithelial-Mesenchymal Transition and Its Clinical Significance in Esophageal Squamous Cell Carcinoma",
abstract = "Objective: The involvement of epithelial-mesenchymal transition (EMT) in esophageal squamous cell carcinoma (ESCC) has not been fully elucidated. Here, we aimed to identify EMT-related genes associated with TGF-β in ESCC and to clarify the role of these genes in the progression of ESCC. Methods: EMT-related genes associated with TGF-β expression were identified in patients with ESCC using microarray analysis and public datasets. The effects of ubiquitin-like with PHD and ring finger domains 2 (UHRF2) expression were analyzed in ESCC cell lines. Cell proliferation and invasion were measured using MTT and invasion assays, respectively. UHRF2 mRNA expression was also analyzed in 75 ESCC specimens to determine the clinical significance of UHRF2 in ESCC. Results: Treatment of ESCC cell lines with TGF-β increased UHRF2 expression. UHRF2 overexpression increased CDH1 (E-cadherin) expression and decreased invasive capacity. The 75 ESCC specimens were divided into the UHRF2 high-expression group (n = 61) and the UHRF2 low-expression group (n = 14). Low UHRF2 expression was significantly correlated with vascular invasion (p = 0.034) and was an independent prognostic factor for poor prognosis (p = 0.005). Conclusion: UHRF2 may be a negative regulator of EMT and a novel prognostic biomarker for ESCC.",
author = "Tomohiro Iguchi and Masami Ueda and Takaaki Masuda and Sho Nambara and Shinya Kidogami and Hisateru Komatsu and Kuniaki Sato and Taro Tobo and Yushi Ogawa and Qingjiang Hu and Tomoko Saito and Hidenari Hirata and Shotaro Sakimura and Ryutaro Uchi and Naoki Hayashi and Shuhei Ito and Hidetoshi Eguchi and Keishi Sugimachi and Yoshihiko Maehara and Koshi Mimori",
note = "Funding Information: This work was supported by the following grants and foundations: Grants-in-Aid for Scientific Research of MEXT (26461980, 15H05791, 26293303, 15H04921, 15K10168, and 15K10170); OITA Cancer Research Foundation; other Grants-in-Aid (GAJJ271004, GAKF900200, and GAKF902600) Funding Information: This work was supported by the following grants and foundations: Grants-in-Aid for Scientific Research of MEXT (26461980, 15H05791, 26293303, 15H04921, 15K10168, and 15K10170); OITA Cancer Research Foundation; other Grants-in-Aid (GAJJ271004, GAKF900200, and GAKF902600). This research used computational resources of the K computer provided by the RIKEN Advanced Institute for Computational Science through the HPCI System Research project (Project ID: hp140230). Computation time was also provided by the Supercomputer System, Human Genome Center, Institute of Medical Science, University of Tokyo (http://sc.hgc.jp/shirokane.html). Clinical samples and corresponding clinical information were provided by Juntendo University Hospital, National Cancer Center Hospital (Tokyo, Japan), Saitama Cancer Center (Saitama, Japan), Kagoshima University Hospital (Kagoshima, Japan), Kyushu University Hospital, Kurume University Hospital (Fukuoka, Japan), and Iwate University School of Medicine (Iwate, Japan). We appreciate the technical support of Ms. Kazumi Oda, Michiko Kasagi, Sachiko Sakuma, Noriko Mishima, and Tomoko Kawano. Publisher Copyright: {\textcopyright} 2018 S. Karger AG, Basel. Copyright: All rights reserved.",
year = "2018",
month = aug,
day = "1",
doi = "10.1159/000488860",
language = "English",
volume = "95",
pages = "179--187",
journal = "Oncology",
issn = "0030-2414",
publisher = "S. Karger AG",
number = "3",
}
