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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Nuclear Mechanotransduction in Cancer Radiation Response: Linking Nuclear Envelope Dynamics to DNA Damage Repair

  • Feiyan Xu1
  • Yang Xiang2
  • Wentian Huang1
  • Ping Hu1,3
  • Shun Wang1
  • Kun Cao1
  • Zhijie Wan1
  • Yanyong Yang1
  • Fu Gao1
  • Yuanyuan Chen1
  1. 1Department of Radiation Medicine, Naval Medical University, Shanghai 200433, China
  2. 2Department of Burns of Changhai Hospital, Naval Medical University, Shanghai 200433, China
  3. 3School of Public Health, China Medical University, Shenyang 110122, China
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Abstract

Tumor mechanics influence radiation response, yet no single mechanical parameter predicts radiosensitivity, and nominally identical variables report opposite results. The gap is not a shortage of mechanisms but the absence of a validated link between a measurable nuclear state, the fidelity of damage processing, and long-term reproductive outcome. This review follows mechanical signals from adhesion and the cytoskeletal systems through the linker of nucleoskeleton and cytoskeleton (LINC) complex, nuclear pores and lamina to chromatin, the nucleolus and DNA repair, asking at each step whether the mechanical input could change how radiation damage is processed rather than how much is produced. Mechanical manipulation combined with irradiation in the same system remains uncommon; most evidence establishes mechanosensitive components without connecting them to a radiation outcome, and this asymmetry accounts for much of the apparent conflict in the literature. We therefore sort the evidence into three levels of support, propose a three-state framework of nuclear mechanical homeostasis (insufficient structural support, maladaptive structural constraint, coordinated integrity and plasticity), and specify the experiments that would falsify it. Nuclear mechanotransduction is better described as a context-dependent adaptive network than as a single determinant of radiosensitivity, and matrix-normalizing, Src-directed and ultrasound-based interventions remain unvalidated for radiotherapy.

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Cite

BibTeXRIS
BibTeX
@article{xu2026nuclear,
  title = {{Nuclear Mechanotransduction in Cancer Radiation Response: Linking Nuclear Envelope Dynamics to DNA Damage Repair}},
  author = {Feiyan Xu and Yang Xiang and Wentian Huang and Ping Hu and Shun Wang and Kun Cao and Zhijie Wan and Yanyong Yang and Fu Gao and Yuanyuan Chen},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27219780},
  url = {https://www.mdpi.com/1422-0067/27/21/9780},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Nuclear Mechanotransduction in Cancer Radiation Response: Linking Nuclear Envelope Dynamics to DNA Damage Repair
AU  - Feiyan Xu
AU  - Yang Xiang
AU  - Wentian Huang
AU  - Ping Hu
AU  - Shun Wang
AU  - Kun Cao
AU  - Zhijie Wan
AU  - Yanyong Yang
AU  - Fu Gao
AU  - Yuanyuan Chen
PY  - 2026
DA  - 2026/10/30
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219780
UR  - https://www.mdpi.com/1422-0067/27/21/9780
AB  - Tumor mechanics influence radiation response, yet no single mechanical parameter predicts radiosensitivity, and nominally identical variables report opposite results. The gap is not a shortage of mechanisms but the absence of a validated link between a measurable nuclear state, the fidelity of damage processing, and long-term reproductive outcome. This review follows mechanical signals from adhesion and the cytoskeletal systems through the linker of nucleoskeleton and cytoskeleton (LINC) complex, nuclear pores and lamina to chromatin, the nucleolus and DNA repair, asking at each step whether the mechanical input could change how radiation damage is processed rather than how much is produced. Mechanical manipulation combined with irradiation in the same system remains uncommon; most evidence establishes mechanosensitive components without connecting them to a radiation outcome, and this asymmetry accounts for much of the apparent conflict in the literature. We therefore sort the evidence into three levels of support, propose a three-state framework of nuclear mechanical homeostasis (insufficient structural support, maladaptive structural constraint, coordinated integrity and plasticity), and specify the experiments that would falsify it. Nuclear mechanotransduction is better described as a context-dependent adaptive network than as a single determinant of radiosensitivity, and matrix-normalizing, Src-directed and ultrasound-based interventions remain unvalidated for radiotherapy.
SN  - 1422-0067
ER  -