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

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.