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Updated: Feb 27, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
TWEAK/Fn14 signaling in tumors
Guanglei Hu1, Weihui Zeng1, Yumin Xia1
1Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
Tumor necrosis factor-related weak inducer of apoptosis (TWEAK) and its receptor Fn14 are upregulated in solid tumors, promoting cancer progression. Targeting this TWEAK/Fn14 pathway shows promise for future cancer therapies.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- TWEAK/Fn14 signaling is implicated in various cellular processes, including cell death, proliferation, and migration.
- Upregulation of TWEAK and Fn14 is observed in numerous solid tumors, suggesting a role in tumorigenesis.
Purpose of the Study:
- To review the role of TWEAK/Fn14 signaling in tumor development.
- To explore TWEAK/Fn14-targeting agents as potential cancer therapeutics.
Main Methods:
- Literature review of studies on TWEAK/Fn14 signaling in cancer.
- Analysis of downstream pathways including TNF receptor-associated factor and NF-kappa B.
- Examination of preclinical and clinical data for TWEAK/Fn14-targeting agents.
Main Results:
- TWEAK/Fn14 activation promotes tumor cell proliferation, invasion, migration, angiogenesis, and epithelial-mesenchymal transitions.
- Targeting agents such as monoclonal antibodies and nanoparticles have shown initial success.
- Downstream signaling pathways are being investigated for novel therapeutic targets.
Conclusions:
- The TWEAK/Fn14 pathway is a critical driver of tumor development.
- Inhibiting TWEAK/Fn14 signaling represents a promising therapeutic strategy for cancer treatment.
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