KEY TAKEAWAYS
- The study aimed to explore H2AZ1’s role and mechanisms in lung cancer progression through various pathways.
- The results showed that H2AZ1 promotes lung cancer progression through the RELA-HIF1A-EGFR signaling pathway.
Histone variants have been shown to play an oncogenic role in cancer progression, but the specific role of H2AZ1 in lung cancer is not fully understood.
Huijie Zhao and the team aimed to investigate H2AZ1’s role and the molecular mechanisms by which it drives lung cancer progression.
Researchers analyzed H2AZ1 expression in lung adenocarcinoma using RNA-seq and microarray datasets. Immunohistochemistry staining for H2AZ1 was performed on two sets of lung cancer tissue microarrays.
To study H2AZ1’s function, they conducted assays for cell proliferation, colony formation, migration, and invasion. In addition, CUT&Tag-seq, ATAC-seq, RNA-seq, and Western blotting were used to examine H2AZ1’s regulatory patterns and potential mechanisms.
The results demonstrated that H2AZ1 is overexpressed in lung cancer, and higher H2AZ1 mRNA levels were linked to worse patient survival. Silencing H2AZ1 reduced cell proliferation, colony formation, migration, and invasion.
Mechanistically, CUT&Tag-seq, ATAC-seq, and RNA-seq data showed that H2AZ1 is primarily located around transcription start sites and impacts various oncogenic pathways. The H2AZ1 was found to promote lung cancer progression via the RELA-HIF1A-EGFR signaling pathway.
The study concluded that H2AZ1 acts as an oncogene in lung cancer by regulating cancer-related pathways, particularly through the RELA-HIF1A-EGFR axis, making it a potential target for precision therapy.
This work was supported in part by the National Natural Science Foundation of China (NSFC) and Shenzhen Municipal Science and Technology Innovation Commission Foundation.
Source: https://pubmed.ncbi.nlm.nih.gov/39327549/
Zhao H, Wu X, Wang Y, et al. (2024). “Histone variant H2AZ1 drives lung cancer progression through the RELA-HIF1A-EGFR signaling pathway.” Cell Commun Signal. 2024;22(1):453. Published 2024 Sep 26. doi:10.1186/s12964-024-01823-3
