Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

• DOI: 10.3892/mmr.2021.12461
• Publication Date: 2021-09-24T05:34:50Z
• Authors: Yujing Huang; Ying Liu; Jing Huang; Lu Gao; Zhenggang Wu; Lu Wang; Lin Fan
• Keywords: Male; 0301 basic medicine; Cell Survival; Gene Expression Profiling; HMGA2 Protein; Computational Biology; Apoptosis; Parkinson Disease; Articles; 3. Good health; Disease Models, Animal; Mice; MicroRNAs; 03 medical and health sciences; Gene Expression Regulation; Cell Line, Tumor; Databases, Genetic; Animals; Humans; RNA Interference; 3' Untranslated Regions

Parkinson's disease (PD), a common multifactorial neurodegenerative disease, is characterized by irreversible loss of dopaminergic neurons in the substantia nigra. In‑depth study of the pathogenesis of PD is of great importance. High‑mobility group AT‑hook 2 (HMGA2) has been proposed to be implicated with neuronal differentiation and impairment of cognitive function. However, whether HMGA2 plays a role in PD is rarely explored. In the present study, N‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP)‑treated PD mice models and N‑methyl‑4‑ phenylpyridinium (MPP+)‑treated SH‑SY5Y cell models were established. Reverse transcription‑quantitative PCR showed that HMGA2 displayed low levels in brain tissues of MPTP‑treated mice and MPP+‑treated SH‑SY5Y cells. Moreover, HMGA2 overexpression suppressed SH‑SY5Y cell apoptosis. Additionally, let‑7b‑5p bound with HMGA2 3' untranslated region (UTR), and its expression was negatively correlated with HMGA2 level. Moreover, let‑7b‑5p presented high levels in brain tissues of PD mice and MPP+‑treated SH‑SY5Y cells, and knockdown of let‑7b‑5p inhibited SH‑SY5Y cell apoptosis. Rescue assays illustrated that HMGA2 neutralized the promotive effects of let‑7b‑5p mimics on SH‑SY5Y cell apoptosis. In conclusion, the present study demonstrated that let‑7b‑5p contributes to cell apoptosis in PD by targeting HMGA2, which offers a potential theoretical basis for the study of effective therapy in PD.