Oncotarget

Research Papers:

Evaluation of cancer-derived myocardial impairments using a mouse model

Yoshihiro Miyagawa, Shota Nukaga, Takuya Mori, Rina Fujiwara-Tani, Kiyomu Fujii, Shiori Mori, Kei Goto, Shingo Kishi, Takamitsu Sasaki, Chie Nakashima, Hitoshi Ohmori, Isao Kawahara, Yi Luo _ and Hiroki Kuniyasu _

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Oncotarget. 2020; 11:3712-3722. https://doi.org/10.18632/oncotarget.27759

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Abstract

Yoshihiro Miyagawa1, Shota Nukaga1,2, Takuya Mori1, Rina Fujiwara-Tani1, Kiyomu Fujii1, Shiori Mori1, Kei Goto1,3, Shingo Kishi1, Takamitsu Sasaki1, Chie Nakashima1, Hitoshi Ohmori1, Isao Kawahara1,2, Yi Luo4 and Hiroki Kuniyasu1

1 Department of Molecular Pathology, Nara Medical University, Kashihara, Nara 634-8521, Japan

2 Division of Rehabilitation, Hanna Central Hospital, Ikoma, Nara 630-0243, Japan

3 Division of Rehabilitation, Hoshida Minami Hospital, Katano, Osaka 576-0022, Japan

4 Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province 226001, China

Correspondence to:

Yi Luo,email: lynantong@hotmail.com
Hiroki Kuniyasu,email: cooninh@zb4.so-net.ne.jp

Keywords: cachexia; myocardium; atrophy; mitochondria; oxidative stress

Received: June 26, 2020     Accepted: September 10, 2020     Published: October 13, 2020

Copyright: © 2020 Miyagawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

ABSTRACT

Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.


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