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Peer-reviewedCC BY 4.0Advanced Science

NUB1 Regulates Muscle Atrophy in Lung Cancer Cachexia via NF‐κB Signaling Pathway

  • Yuqi Han1,2,3
  • Yaru Xia1
  • Weiquan Li2,3
  • Jiaming Wu1
  • Tiexi Yu2,3
  • Diaoyi Tan2,3
  • Daojia Miao2,3
  • Wen Li1
  • Xuejiao Dong1
  • Jiemin Li1
  • Yu Jiao1
  • Guixiao Huang4
2 more authors
  • Xiaoping Zhang2,3,5
  • Hongmei Yang1
5 affiliations
  1. 1Department of Pathogenic Biology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology Wuhan China
  2. 2Department of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China
  3. 3Institute of Urology Tongji Medical College Huazhong University of Science and Technology Wuhan China
  4. 4Department of Urology The Third Affiliated Hospital of Shenzhen University: Shenzhen Luohu Hospital Group Luohu People's Hospital Shenzhen China
  5. 5Shenzhen Huazhong University of Science and Technology Research Institute Shenzhen China
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Abstract

Cancer‐associated cachexia (CAC) is a devastating multifactorial syndrome characterized by progressive skeletal muscle atrophy. Its mechanisms remain incompletely clarified, with limited effective therapeutic targets. NUB1, a negative regulator of ubiquitin‐like proteins mediating protein degradation, has not been fully elucidated in CAC‐induced muscle atrophy. Here, NUB1 was significantly upregulated in skeletal muscles of Lewis lung carcinoma (LLC) cachexia mice and C2C12 myotube atrophy models stimulated with LLC tumor‐conditioned medium (LCM). Silencing NUB1 alleviated LCM‐induced myotube atrophy in vitro and enhanced muscle mass, fiber cross‐sectional area and function in LLC cachectic mice in vivo. Mechanistically, upregulated NUB1 recruited IκBα to bind proteasomal subunit S5a, promoting IκBα degradation, thus increasing NF‐κB nuclear translocation and transcription of Atrogin1 and MuRF1. Silencing NUB1 inhibited NF‐κB activation, while TNFα reversed its protective effect. These findings identified NUB1 as a novel driver of CAC‐related muscle atrophy and highlighted the NUB1/IκBα/NF‐κB axis as a promising therapeutic target.

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Cite

BibTeXRIS
BibTeX
@article{han2026nub1,
  title = {{NUB1 Regulates Muscle Atrophy in Lung Cancer Cachexia via NF‐κB Signaling Pathway}},
  author = {Yuqi Han and Yaru Xia and Weiquan Li and Jiaming Wu and Tiexi Yu and Diaoyi Tan and Daojia Miao and Wen Li and Xuejiao Dong and Jiemin Li and Yu Jiao and Guixiao Huang and Xiaoping Zhang and Hongmei Yang},
  journal = {Advanced Science},
  year = {2026},
  month = oct,
  doi = {10.1002/advs.78492},
  url = {https://doi.org/10.1002/advs.78492},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - NUB1 Regulates Muscle Atrophy in Lung Cancer Cachexia via NF‐κB Signaling Pathway
AU  - Yuqi Han
AU  - Yaru Xia
AU  - Weiquan Li
AU  - Jiaming Wu
AU  - Tiexi Yu
AU  - Diaoyi Tan
AU  - Daojia Miao
AU  - Wen Li
AU  - Xuejiao Dong
AU  - Jiemin Li
AU  - Yu Jiao
AU  - Guixiao Huang
AU  - Xiaoping Zhang
AU  - Hongmei Yang
PY  - 2026
DA  - 2026/10/31
JO  - Advanced Science
DO  - 10.1002/advs.78492
UR  - https://doi.org/10.1002/advs.78492
AB  - Cancer‐associated cachexia (CAC) is a devastating multifactorial syndrome characterized by progressive skeletal muscle atrophy. Its mechanisms remain incompletely clarified, with limited effective therapeutic targets. NUB1, a negative regulator of ubiquitin‐like proteins mediating protein degradation, has not been fully elucidated in CAC‐induced muscle atrophy. Here, NUB1 was significantly upregulated in skeletal muscles of Lewis lung carcinoma (LLC) cachexia mice and C2C12 myotube atrophy models stimulated with LLC tumor‐conditioned medium (LCM). Silencing NUB1 alleviated LCM‐induced myotube atrophy in vitro and enhanced muscle mass, fiber cross‐sectional area and function in LLC cachectic mice in vivo. Mechanistically, upregulated NUB1 recruited IκBα to bind proteasomal subunit S5a, promoting IκBα degradation, thus increasing NF‐κB nuclear translocation and transcription of Atrogin1 and MuRF1. Silencing NUB1 inhibited NF‐κB activation, while TNFα reversed its protective effect. These findings identified NUB1 as a novel driver of CAC‐related muscle atrophy and highlighted the NUB1/IκBα/NF‐κB axis as a promising therapeutic target.
SN  - 2198-3844
ER  -