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Scutellarein attenuates cancer cachexia-induced muscle atrophy via targeted inhibition of the JAK/STAT pathway

斯达 肌肉萎缩 癌症恶病质 癌症研究 恶病质 萎缩 JAK-STAT信号通路 医学 癌症 内科学 信号转导 生物 细胞生物学 车站3 受体 酪氨酸激酶
作者
Hye Seong Ahn,Hyun Woo Kim,Yang‐Suk Yoon,Minju Jeong,Sieun Lee,Peng Chen,Keke Wang,Sujung Park,Jae Hwan Kim,Jiyun Ahn,Qiantao Wang,Yoonhee Jin,Young Jin Jang,Sanguine Byun
出处
期刊:Journal of Advanced Research [Elsevier BV]
标识
DOI:10.1016/j.jare.2025.07.001
摘要

Cancer cachexia is a multifaceted metabolic syndrome characterized by severe loss of skeletal muscle and adipose tissue, diminishing both quality of life and survival in cancer patients. Despite its prevalence, effective treatments for cancer cachexia remain limited. The JAK/STAT signaling pathway has been identified as a key driver of muscle atrophy in cachexia. This study aimed to investigate the therapeutic potential of scutellarein, a natural compound, as a JAK kinase inhibitor to prevent and mitigate cancer cachexia-induced muscle atrophy. In vitro experiments were conducted using the mouse myoblast cell line C2C12 and human induced pluripotent stem cell (hiPSC)-derived skeletal muscle cells. Myotube atrophy was induced using IFN-γ/TNF-α and cancer cell-conditioned media. Two independent mouse models of cancer cachexia were utilized for in vivo analysis. Muscle tissues were examined through transcriptomic and molecular analyses, including RNA sequencing, PCR, and immunoblotting. Structure-activity relationship studies and molecular docking analyses were performed to investigate the binding interaction of scutellarein with JAK kinases. Through a chemical library screen, we identified scutellarein as a potent JAK kinase inhibitor. Scutellarein effectively mitigated myotube atrophy by inhibiting protein degradation and promoting protein synthesis in C2C12 and hiPSC-derived muscle cells. In two distinct mouse models of cancer cachexia, scutellarein treatment significantly reduced muscle wasting, improved muscle strength and function, and countered fat depletion. Transcriptomic and molecular analyses of muscle tissues further demonstrated that scutellarein inhibited activation of JAK/STAT pathways and restored suppression of myogenesis and mitochondrial biogenesis. Structure-activity relationship analyses further revealed critical hydroxyl group positions essential for JAK binding. Collectively, our findings suggest scutellarein as a promising candidate for the prevention and treatment of cancer cachexia, providing a novel therapeutic approach to address this critical unmet need in cancer care.
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