Long non‐coding RNA MALAT1 regulates cell proliferation and apoptosis via miR-135b-5p/GPNMB axis in Parkinson’s disease cell model

Biological Research

Yanbing Zheng¹  Yuhua Liu¹  Peifeng Yin¹  Shaowen Dai¹  Haifeng Miao¹  Kefeng Lv² 

[1] Department of General Practice, Affiliated Dongguan People’s Hospital, Southern Medical University (Dongguan People’s Hospital), 3 South Wandao Road, Wanjiang District, 523059, Dongguan, Guangdong Province, People’s Republic of China;Department of Neurology, Affiliated Dongguan People’s Hospital, Southern Medical University (Dongguan People’s Hospital), 523059, Dongguan, Guangdong Province, People’s Republic of China;

关键词: MALAT1;    miR-135b-5p;    GPNMB;    Parkinson’s disease;    Cell proliferation;    Apoptosis;   

DOI  :  10.1186/s40659-021-00332-8

来源: Springer

【 摘 要 】

BackgroundsParkinson’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.MethodsSK-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.ResultsMALAT1 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.ConclusionOur 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.

【 授权许可】

CC BY