ArticleCell death discovery2022
Inhibition of Rac1 attenuates radiation-induced lung injury while suppresses lung tumor in mice.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- HOXA10 drives immune evasion in early lung adenocarcinoma by recruiting immunosuppressive macrophages via NF-κB/CCL2 signaling.Journal of experimental & clinical cancer research : CR · 2026Article
- Investigation of the protective effect of cilostazol on acute lung injury-mediated inflammation and in silico molecular modelling studies of inflammatory signalling pathway: a repurposing study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Molecular mechanisms of lung injury from ultra high and conventional dose rate pulsed radiation based on 4D DIA proteomics study.Scientific reports · 2025Article
- N-Cadherin based adhesion and Rac1 activity regulate tension polarization in the actin cortex.Scientific reports · 2025Article
- Review
- Inhalable CAR-T cell-derived exosomes as paclitaxel carriers for treating lung cancer.Journal of translational medicine · 2023Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.