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Open AccessArticle

Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia

1
Exercise Science Research Center, Cachexia Research Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR 72701, USA
2
Integrative Physiology and Nutrition Laboratory Name, Department of Health and Kinesiology, University of Texas at Tyler, Tyler, TX 75799, USA
3
Exercise Science Research Center, Exercise Muscle Biology Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR 72701, USA
4
Department of Health, Human Performance and Recreation, Baylor University, Waco, TX 76798, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(21), 7841; https://doi.org/10.3390/ijms21217841
Received: 24 September 2020 / Revised: 15 October 2020 / Accepted: 20 October 2020 / Published: 22 October 2020
(This article belongs to the Special Issue Muscle Atrophy: Discovery of Mechanisms and Potential Therapies)
It is established that cancer cachexia causes limb muscle atrophy and is strongly associated with morbidity and mortality; less is known about how the development of cachexia impacts the diaphragm. The purpose of this study was to investigate cellular signaling mechanisms related to mitochondrial function, reactive oxygen species (ROS) production, and protein synthesis during the development of cancer cachexia. C57BL/J6 mice developed Lewis Lung Carcinoma for either 0 weeks (Control), 1 week, 2 weeks, 3 weeks, or 4 weeks. At designated time points, diaphragms were harvested and analyzed. Mitochondrial respiratory control ratio was ~50% lower in experimental groups, which was significant by 2 weeks of cancer development, with no difference in mitochondrial content markers COXIV or VDAC. Compared to the controls, ROS was 4-fold elevated in 2-week animals but then was not different at later time points. Only one antioxidant protein, GPX3, was altered by cancer development (~70% lower in experimental groups). Protein synthesis, measured by a fractional synthesis rate, appeared to become progressively lower with the cancer duration, but the mean difference was not significant. The development and progression of cancer cachexia induces marked alterations to mitochondrial function and ROS production in the diaphragm and may contribute to increased cachexia-associated morbidity and mortality. View Full-Text
Keywords: protein synthesis; protein degradation; muscle atrophy; mitochondrial function; mTOR; oxidative stress; FOXO protein synthesis; protein degradation; muscle atrophy; mitochondrial function; mTOR; oxidative stress; FOXO
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MDPI and ACS Style

Rosa-Caldwell, M.E.; Benson, C.A.; Lee, D.E.; Brown, J.L.; Washington, T.A.; Greene, N.P.; Wiggs, M.P. Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia. Int. J. Mol. Sci. 2020, 21, 7841. https://doi.org/10.3390/ijms21217841

AMA Style

Rosa-Caldwell ME, Benson CA, Lee DE, Brown JL, Washington TA, Greene NP, Wiggs MP. Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia. International Journal of Molecular Sciences. 2020; 21(21):7841. https://doi.org/10.3390/ijms21217841

Chicago/Turabian Style

Rosa-Caldwell, Megan E.; Benson, Conner A.; Lee, David E.; Brown, Jacob L.; Washington, Tyrone A.; Greene, Nicholas P.; Wiggs, Michael P. 2020. "Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia" Int. J. Mol. Sci. 21, no. 21: 7841. https://doi.org/10.3390/ijms21217841

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