Article · Volume 21, Issue 3 · pp. 895–905

Luteolin-Zinc Modulates PRR11 Methylation and Ferroptosis in Lung Cancer Cells Under Hypoxia

Jiayong Huang¹, Binbo Fang², Ting Guo², Yiyang Li², Yilin Yang², Jiongcheng Ying², Haoyun Zhou², Xiang Li¹

¹Department of Respiratory Medicine, Yuhuan Second People’s Hospital, Yuhuan, Taizhou, CHINA.
²Department of Medicine, Taizhou University, Jiaojiang, Zhejiang, China.

Abstract

Background: Activation of PRR11 contributes to the progression of lung cancer and is related to its methylation status. However, the regulatory mechanism of luteolin-zinc (Lu-Zn) on PRR11 methylation-mediated lung cancer progression under hypoxic conditions remains to be explored.Objectives: This study aims to investigate the inhibitory effect of Lu-Zn on lung cancer cells, its regulation of ferroptosis, and the role of PRR11 in lung cancer progression under hypoxia.Materials and Methods: In vitro experiments were conducted to evaluate the effect of Lu-Zn on lung cancer cells, focusing on its impact on invasion, migration, and ferroptosis. The expression levels of PRR11, its methylation status, and microRNA- 6769b-3p (miR-6769b-3p) were also analyzed.Results: Under hypoxic conditions, Lu-Zn significantly inhibited the invasion and migration abilities of lung cancer cells and promoted ferroptosis. Additionally, Lu-Zn reversed the pro-cancer effects induced by PRR11. At the molecular level, Lu-Zn promoted the methylation of PRR11 and regulated miR-6769b-3p.Conclusion: Our study demonstrates that Lu-Zn enhances the methylation of PRR11 and reduces its expression under hypoxic conditions through miR-6769b-3p. This leads to inhibition of the downstream PI3K/AKT/mTOR signaling pathway, promoting ferroptosis and exerting anti-lung cancer effects.

Keywords: Luteolin-zinc; ferroptosis; PRR11; methylation; hypoxia; lung cancer

The full text of this article is available as a PDF. Open the PDF.