Abstract: OBJECTIVE：To explore the impacts of the long non-coding RNA (lncRNA) HOX transcript antisense RNA，myeloid-specific 1 (HOTAIRM1)，on the vitality and apoptosis of MN9D cells which were induced by 1-methyl-4-phenylpyridinium ion ([MPP⁺]). METHODS：MN9D cells were treated with different concentrations (0，0.25，0.5，1，1.25，2.5 mmol/L) of MPP⁺ for various time periods (0，24，48，and 72 h). Subsequently，cell viability of each group was evaluated using the CCK-8 assay. Based on the results，the optimal concentration of MPP⁺ and the most appropriate treatment duration were determined for subsequent experiments. siRNA transfections were conducted. The MN9D cells were then categorized into the control group，MPP⁺ group，si-NC+MPP⁺ group，and si-HOTAIRM1+MPP⁺ group. Cell viability of each group was measured by CCK-8 assay. Expression of lncRNA HOTAIRM1 was detected through real-time fluorescent quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Apoptosis status was analyzed by flow cytometry. RESULTS：In comparison with the control group，lncRNA HOTAIRM1 was highly expressed in MN9D cells induced by MPP⁺ (P<0.05). When treated with 1 mmol/L MPP⁺ for 24 h，the cell viability was significantly decreased，while the expression level of lncRNA HOTAIRM1 was remarkably elevated. Hence，1 mmol/L MPP⁺ for 24 h treatment was selected for subsequent experiments. After the induction and siRNA interference，expression of lncRNA HOTAIRM1 was significantly reduced (P<0.001)，and viability of the cells were significantly enhanced (P<0.01). Knockdown of lncRNA HOTAIRM1 inhibited the apoptosis of the induced cells (P<0.01). CONCLUSION：Interfering with the expression of lncRNA HOTAIRM1 augmented viability of the MN9D cells induced by MPP⁺ and suppressed cell apoptosis. Knockdown of lncRNA HOTAIRM1 exerted a protective effect on the induced cells.

Key words: MN9D cell, Parkinson's disease, long non-coding RNA, HOTAIRM1, apoptosis