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Deterioration in Muscle Mass and Physical Function Differs According to Weight Loss History in Cancer Cachexia
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ER Stress and Unfolded Protein Response in Cancer Cachexia

Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA
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Cancers 2019, 11(12), 1929; https://doi.org/10.3390/cancers11121929
Received: 2 November 2019 / Revised: 26 November 2019 / Accepted: 30 November 2019 / Published: 3 December 2019
(This article belongs to the Special Issue Cancer Cachexia)
Cancer cachexia is a devastating syndrome characterized by unintentional weight loss attributed to extensive skeletal muscle wasting. The pathogenesis of cachexia is multifactorial because of complex interactions of tumor and host factors. The irreversible wasting syndrome has been ascribed to systemic inflammation, insulin resistance, dysfunctional mitochondria, oxidative stress, and heightened activation of ubiquitin-proteasome system and macroautophagy. Accumulating evidence suggests that deviant regulation of an array of signaling pathways engenders cancer cachexia where the human body is sustained in an incessant self-consuming catabolic state. Recent studies have further suggested that several components of endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) are activated in skeletal muscle of animal models and muscle biopsies of cachectic cancer patients. However, the exact role of ER stress and the individual arms of the UPR in the regulation of skeletal muscle mass in various catabolic states including cancer has just begun to be elucidated. This review provides a succinct overview of emerging roles of ER stress and the UPR in cancer-induced skeletal muscle wasting.
Keywords: Skeletal muscle; cancer cachexia; ER stress; PERK; IRE1; ATF4; XBP1; ATF6; and signaling. Skeletal muscle; cancer cachexia; ER stress; PERK; IRE1; ATF4; XBP1; ATF6; and signaling.
MDPI and ACS Style

Roy, A.; Kumar, A. ER Stress and Unfolded Protein Response in Cancer Cachexia. Cancers 2019, 11, 1929.

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