LncRNA NEAT1 promoted MPP+‑induced ferroptosis via regulating miR‑150‑5p/BAP1 pathway in SK‑N‑SH cells.

As widely reported, dysregulated ferroptosis is closely associated with Parkinson's disease (PD) progression. The goal of the present study was to probe the roles of long non‑coding RNA (lncRNA) nuclear enriched assembly transcript 1 (NEAT1) in regulating ferroptosis in PD. PD cell model was constructed by subjecting SK‑N‑SH cells to 1‑methyl‑4‑phenylpyridinium (MPP+) for 24 h. The RNA levels of NEAT1, miRNA (miR)‑150‑5p, and BRCA1‑associated protein 1 (BAP1) were evaluated using qRT‑PCR. The protein levels of glutathione peroxidase 4 (GPX4), BAP1, and solute carrier family 7 member 11 (SLC7A11) were determined using western blot. Cell viability was assessed using 3‑(4,5‑dimethylthiazolyl2)‑2, 5‑diphenyltetrazolium bromide (MTT) assay. In addition, fluorescent probe 2,7‑dichlorodihydrofluorescein diacetate (DCFH‑DA) was employed to determine the ROS level. Moreover, the levels of GSH, MDA, and Fe2+ were also measured. Finally, the interactions among NEAT1, miR‑150‑5p, and BAP1 were identified by dual luciferase reporter gene assay, and/or RIP assay. Upregulated NEAT1 was observed in PD cell model. Knockdown of NEAT1 elevated viability and GSH level in PD cell model and reduced ROS, MDA, and Fe2+ levels. Moreover, NEAT1 functioned as a sponge to suppress miR‑150‑5p expression. Moreover, miR‑150‑5p overexpression suppressed ferroptosis in PD cell model. We subsequently found that miR‑150‑5p regulated SLC7A11 expression by directly binding to BAP1. miR‑150‑5p inhibition or BAP1 overexpression mitigated the anti‑ferroptosis effect meditated by sh‑NEAT1. Taken together, knockdown of NEAT1 mitigated MPP+‑induced ferroptosis through regulating BAP1/SLC7A11 axis by sponging miR‑150‑5p, indicating the potential of NEAT1 as a promising therapeutic target for PD.