HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >

KDM2B promotes cell viability by enhancing DNA damage response in canine hemangiosarcoma

This item is licensed under:Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International

Files in This Item:
JGG-D-21-00118R3-edited KA 20210511.pdf3.42 MBPDFView/Open
Supplementary file Gulay et al for JGG 20210305.pdfSupplementary file1.83 MBPDFView/Open
Please use this identifier to cite or link to this item:

Title: KDM2B promotes cell viability by enhancing DNA damage response in canine hemangiosarcoma
Authors: Gulay, Kevin Christian Montecillo Browse this author
Aoshima, Keisuke Browse this author
Shibata, Yuki Browse this author
Yasui, Hironobu Browse this author →KAKEN DB
Yan, Qin Browse this author
Kobayashi, Atsushi Browse this author
Kimura, Takashi Browse this author →KAKEN DB
Keywords: DNA repair
Issue Date: 20-Jul-2021
Publisher: Science Press
Journal Title: Journal of Genetics and Genomics
Volume: 48
Issue: 7
Start Page: 618
End Page: 630
Publisher DOI: 10.1016/j.jgg.2021.02.005
Abstract: Epigenetic regulators have been implicated in tumorigenesis of many types of cancer; however, their roles in endothelial cell cancers such as canine hemangiosarcoma (HSA) have not been studied. In this study, we find that lysine-specific demethylase 2b (KDM2B) is highly expressed in HSA cell lines compared with normal canine endothelial cells. Silencing of KDM2B in HSA cells results in increased cell death in vitro compared with the scramble control by inducing apoptosis through the inactivation of the DNA repair pathways and accumulation of DNA damage. Similarly, doxycycline-induced KDM2B silencing in tumor xenografts results in decreased tumor sizes compared with the control. Furthermore, KDM2B is also highly expressed in clinical cases of HSA. We hypothesize that pharmacological KDM2B inhibition can also induce HSA cell death and can be used as an alternative treatment for HSA. We treat HSA cells with GSK-J4, a histone demethylase inhibitor, and find that GSK-J4 treatment also induces apoptosis and cell death. In addition, GSK-J4 treatment decreases tumor size. Therefore, we demonstrate that KDM2B acts as an oncogene in HSA by enhancing the DNA damage response. Moreover, we show that histone demethylase inhibitor GSK-J4 can be used as a therapeutic alternative to doxorubicin for HSA treatment. Copyright (C) 2021, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, and Genetics Society of China. Published by Elsevier Limited and Science Press. All rights reserved.
Rights: © <2021>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 青島 圭佑

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 - Hokkaido University