Abstract

Cancer cachexia (CC) is a complicated metabolic derangement and muscle wasting syndrome, affecting 50–80% cancer patients. So far, molecular mechanisms underlying CC remain elusive. Metabolomics techniques have been used to study metabolic shifts including changes of metabolite concentrations and disturbed metabolic pathways in the progression of CC, and expand further fundamental understanding of muscle loss. In this article, we aim to review the research progress and applications of metabolomics on CC in the past decade, and provide a theoretical basis for the study of prediction, early diagnosis, and therapy of CC.

Highlights

  • Cancer cachexia (CC) is a multifactorial syndrome, which is characterized by disturbed metabolism, declined body weight, depleted muscle mass, and reduced food intake (Evans et al, 2008; Fearon et al, 2011)

  • To widely expand the knowledge of CC and give inspirations for the cachexia studies from the view of biomarkers, signatures and therapeutic targets, we focus on the progress made in the past decade, novel developments, and latest discoveries in the study of CC using metabolomic techniques, and look forward to its future developments

  • Our results indicated that significantly impaired pathways including energy metabolism, muscle protein breakdown and synthesis, and profoundly increased amino acids involved in tricarboxylic acid (TCA) cycle anaplerotic

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Summary

Introduction

Cancer cachexia (CC) is a multifactorial syndrome, which is characterized by disturbed metabolism, declined body weight, depleted muscle mass, and reduced food intake (Evans et al, 2008; Fearon et al, 2011). CC begins in a pre-cachexia stage with unwitting body weight loss, along with a more severe and noninvertible fat tissues and skeletal muscles loss, followed by disturbances in metabolic pathway and immune system, resulting in death (Hamerman, 2002; Deans et al, 2009). Declined body weight primarily arise from skeletal muscle loss, which is recognized as the major feature of CC. Several major signaling pathways including IGF1-Akt-FoxO pathway, TGFβ-myostatin pathway, NF-κB signaling, and glucocorticoids pathway have all been implicated in muscle atrophy of CC (Bodine et al, 2001; Musaro et al, 2001; Lee, 2004; Sandri et al, 2004; Waddell et al, 2008; Peterson et al, 2011).

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