Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
[Molecular Mechanism of microRNA-429 Targeting HMOX1 to Regulate Invasion, Migration, and Ferroptosis in Lung Adenocarcinoma Cells].
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Gao Xinyu, Gong Xiuying, Hou Shunfu, Zhang Zhihan, Li Hongli, Wang Xuejing
Аннотация
OBJECTIVE: To investigate the effects of microRNA-429 (miR-429) on the invasion, migration, and ferroptosis of lung adenocarcinoma (LUAD) cells, and to provide new insights into the clinical inhibition of LUAD invasion and migration and the promotion of ferroptosis.
METHODS: The expression profile of miR-429 in LUAD tissues was analyzed using the starBase database. Quantitative real-time PCR (qRT-PCR) was performed to assess miR-429 expression levels in normal human bronchial epithelial cells (the BEAS-2B cell line) and LUAD cells (the A549 and H1975 cell lines), and to evaluate the plasmid transfection efficiency. The effects of miR-429 on A549 cell proliferation, migration, and invasion were assessed using 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay, scratch wound healing assay, and Transwell invasion assay, respectively. Potential ferroptosis-related proteins targeted by miR-429 were predicted using bioinformatics databases, and the targeting relationship between miR-429 and heme oxygenase 1 (HMOX1) was validated by a dual-luciferase reporter assay. Further functional experiments were performed to examine the effect of miR-429 targeting HMOX1 on the malignant phenotypes of A549 cells. The levels of reactive oxygen species (ROS) and lipid ROS (L-ROS) were measured to analyze the regulatory effects of miR-429 and HMOX1 on oxidative stress in LUAD cells. The contents of malondialdehyde (MDA), glutathione (GSH), and ferrous ion (Fe2+) were measured to evaluate evaluate the effects of miR-429 and HMOX1 on key ferroptosis-associated indicators in LUAD cells.
RESULTS: miR-429 expression was significantly higher in LUAD cell lines (A549 and H1975) compared with that in normal cells (BEAS-2B), with the highest expression level observed in A549 cells. Functional experiments demonstrated that miR-429 promoted A549 cell proliferation, migration, and invasion. The dual-luciferase assay confirmed that miR-429 directly targeted HMOX1, and their expression levels were negatively correlated in LUAD cells. HMOX1 overexpression inhibited the proliferation, invasion, and migration of A549 cells, while miR-429 overexpression reversed these inhibitory effects. Mechanistically, miR-429 targeted and inhibited HMOX1, which led to reduced intracellular levels of ROS, L-ROS, MDA, and Fe2+ and increased GSH levels in A549 cells, thereby decreasing cellular sensitivity to ferroptosis.
CONCLUSION: miR-429 promotes the invasion and migration of LUAD cells and inhibits ferroptosis by targeting and inhibiting HMOX1.
METHODS: The expression profile of miR-429 in LUAD tissues was analyzed using the starBase database. Quantitative real-time PCR (qRT-PCR) was performed to assess miR-429 expression levels in normal human bronchial epithelial cells (the BEAS-2B cell line) and LUAD cells (the A549 and H1975 cell lines), and to evaluate the plasmid transfection efficiency. The effects of miR-429 on A549 cell proliferation, migration, and invasion were assessed using 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay, scratch wound healing assay, and Transwell invasion assay, respectively. Potential ferroptosis-related proteins targeted by miR-429 were predicted using bioinformatics databases, and the targeting relationship between miR-429 and heme oxygenase 1 (HMOX1) was validated by a dual-luciferase reporter assay. Further functional experiments were performed to examine the effect of miR-429 targeting HMOX1 on the malignant phenotypes of A549 cells. The levels of reactive oxygen species (ROS) and lipid ROS (L-ROS) were measured to analyze the regulatory effects of miR-429 and HMOX1 on oxidative stress in LUAD cells. The contents of malondialdehyde (MDA), glutathione (GSH), and ferrous ion (Fe2+) were measured to evaluate evaluate the effects of miR-429 and HMOX1 on key ferroptosis-associated indicators in LUAD cells.
RESULTS: miR-429 expression was significantly higher in LUAD cell lines (A549 and H1975) compared with that in normal cells (BEAS-2B), with the highest expression level observed in A549 cells. Functional experiments demonstrated that miR-429 promoted A549 cell proliferation, migration, and invasion. The dual-luciferase assay confirmed that miR-429 directly targeted HMOX1, and their expression levels were negatively correlated in LUAD cells. HMOX1 overexpression inhibited the proliferation, invasion, and migration of A549 cells, while miR-429 overexpression reversed these inhibitory effects. Mechanistically, miR-429 targeted and inhibited HMOX1, which led to reduced intracellular levels of ROS, L-ROS, MDA, and Fe2+ and increased GSH levels in A549 cells, thereby decreasing cellular sensitivity to ferroptosis.
CONCLUSION: miR-429 promotes the invasion and migration of LUAD cells and inhibits ferroptosis by targeting and inhibiting HMOX1.