Parkinson’s disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. SK-N-SH and SK-N-BE cells were treated with MPP+ to establish the MPP+-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP+-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP+-stimulated cell model of PD were explored. MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP+-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP+-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.

中文翻译：

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较长的非编码RNA MALAT1通过miR-135b-5p / GPNMB轴调节帕金森病细胞模型中的细胞增殖和凋亡

帕金森氏病（PD）是世界范围内常见的与年龄相关的神经退行性疾病。这项研究旨在调查长期的非编码RNA转移相关的肺腺癌转录本1（MALAT1）在PD中的作用和机制。用MPP +处理SK-N-SH和SK-N-BE细胞，建立MPP +刺激的PD细胞模型，并测定MALAT1表达。然后，在MPP +刺激的PD细胞模型中确定了MALAT1耗竭对细胞增殖和凋亡的影响。此外，还探讨了在MPP +刺激的PD细胞模型中，microRNA-135b-5p（miR-135b-5p）与MALAT1或糖蛋白非转移性黑色素瘤蛋白B（GPNMB）之间的相关性。MALAT1越来越多地表达，而MALAT1的下调促进了细胞增殖，同时抑制了MPP +刺激的细胞的凋亡。除了，miR-135b-5p是MALAT1的靶标，直接靶向GPNMB。进一步的研究表明，通过miR-135b-5p / GPNMB轴抑制MALAT1可以调节细胞增殖和凋亡。我们的发现表明，MALAT1 / miR-135b-5p / GPNMB轴调节了MPP +刺激的PD细胞模型中的细胞增殖和凋亡，为PD提供了潜在的生物标志物和治疗靶标。