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Merck
CN
  • Sevoflurane attenuate hypoxia-induced VEGF level in tongue squamous cell carcinoma cell by upregulating the DNA methylation states of the promoter region.

Sevoflurane attenuate hypoxia-induced VEGF level in tongue squamous cell carcinoma cell by upregulating the DNA methylation states of the promoter region.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (2015-05-12)
Yi Lu, Jing Wang, Jia Yan, Yaqiong Yang, Yu Sun, Yan Huang, Rong Hu, Ying Zhang, Hong Jiang
摘要

Anaesthetic agents were confirmed to play a role on the tumor angiogenesis. The effect of sevoflurane on tongue squamous cell carcinoma (TSCC) cell has not been investigated. SCC-4 cells were exposed to sevoflurane after simulating hypoxia. Then, both the mRNA and protein level of hypoxia-inducible factor (HIF)-1α and VEGF were detected. The methylation states of the VEGF promoter region were also assessed to reveal the underlying mechanism. Finally, the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-Aza) was administrated to reveal the relationship of DNA methylation on the regulation of the VEGF level. Results showed that sevoflurane attenuated the hypoxia-induced VEGF level without altering the HIF-1α after exposure for 24 and 72 h. Sevoflurane increased the DNA methylation of the VEGF promoter region. The attenuation effect of sevoflurane on hypoxia-induced VEGF level could be blocked by 5-Aza. We concluded that sevoflurane attenuates hypoxia-induced VEGF level via DNA methylation of the promoter region in TSCC cell.

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