Abstract
Muscle cachexia is one of the most critical unmet medical needs. Identifying the molecular background of cancer-induced muscle loss revealed a promising possibility of new therapeutic targets and new drug development. In this review, we will define the signal transducer and activator of transcription 3 (STAT3) protein's role in the tumor formation process and summarize the role of STAT3 in skeletal muscle cachexia. Finally, we will discuss a vast therapeutic potential for the STAT3-inhibiting single-agent treatment innovation that, as the desired outcome, could block tumor growth and generally prevent muscle cachexia.
Keywords:
muscle cachexia; pSTAT3 inhibitors; targeted therapy.
MeSH terms
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Animals
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Cachexia / drug therapy*
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Cachexia / etiology
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Cachexia / metabolism
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Humans
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Janus Kinase 2* / antagonists & inhibitors
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Janus Kinase 2* / metabolism
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Janus Kinase 2* / physiology
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Molecular Targeted Therapy / methods*
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Molecular Targeted Therapy / trends
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Muscle, Skeletal / metabolism
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Muscle, Skeletal / pathology
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Muscular Atrophy / drug therapy*
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Muscular Atrophy / etiology
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Muscular Atrophy / metabolism
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Neoplasms / complications
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Neoplasms / drug therapy
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Neoplasms / metabolism
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Neoplasms / pathology
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Phosphorylation / drug effects
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Protein Kinase Inhibitors / pharmacology
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STAT3 Transcription Factor* / antagonists & inhibitors
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STAT3 Transcription Factor* / metabolism
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STAT3 Transcription Factor* / physiology
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Signal Transduction / drug effects
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Signal Transduction / physiology
Substances
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Protein Kinase Inhibitors
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STAT3 Transcription Factor
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STAT3 protein, human
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JAK2 protein, human
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Janus Kinase 2