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Smoking-associated upregulation of CBX3 suppresses ARHGAP24 expression to activate Rac1 signaling and promote tumor progression in lung adenocarcinoma
Smoking-associated upregulation of CBX3 suppresses ARHGAP24 expression to activate Rac1 signaling and promote tumor progression in lung adenocarcinoma
- Source :
- Oncogene
- Publication Year :
- 2021
- Publisher :
- Springer Science and Business Media LLC, 2021.
-
Abstract
- Although tobacco smoking is a risk factor for lung adenocarcinoma (LUAD), the mechanisms by which tobacco smoking induces LUAD development remain elusive. Histone methylation levels in human bronchial epithelial cells have been reported to increase after exposure to cigarettes. In this study, we explored the mechanisms regulating histone methylation in LUAD in response to smoking. We found that the histone H3K9 methylation reader CBX3 was upregulated in current smokers with LUAD, and that CBX3 overexpression promoted LUAD progression. Functional enrichment analyses revealed that CBX3 regulated the activation of Rho GTPases in LUAD. We also found that by forming a complex with TRIM28, TRIM24, and RBBP4, CBX3 repressed the expression of ARHGAP24 and increased the amount of active Rac1 in LUAD cells. Collectively, these results suggest that smoking associated upregulation of CBX3 promotes LUAD progression by activating the ARHGAP24/Rac1 pathway. Hence, the CBX3/ARHGAP24/Rac1 axis may represent a promising therapeutic target in smoking-induced LUAD.
- Subjects :
- rac1 GTP-Binding Protein
Cancer Research
Lung Neoplasms
TRIM28
Chromosomal Proteins, Non-Histone
Mice, Nude
Adenocarcinoma of Lung
RAC1
Biology
Article
TRIM24
Mice
Downregulation and upregulation
Cell Line, Tumor
Histone methylation
Tobacco Smoking
Genetics
medicine
Animals
Humans
Molecular Biology
GTPase-Activating Proteins
Oncogenes
medicine.disease
Up-Regulation
Histone
Tumor progression
Cancer research
biology.protein
Adenocarcinoma
Non-small-cell lung cancer
Subjects
Details
- ISSN :
- 14765594 and 09509232
- Volume :
- 41
- Database :
- OpenAIRE
- Journal :
- Oncogene
- Accession number :
- edsair.doi.dedup.....70ec8b901cbace3e0d3977345fa57bbe
- Full Text :
- https://doi.org/10.1038/s41388-021-02114-8