MiR-142-5p Protects Against 6-OHDA-Induced SH-SY5Y Cell Injury by Downregulating BECN1 and Autophagy

BACKGROUND: MiR-142-5p has been demonstrated to hold significant implications in neurological diseases. However, the impact and underlying regulatory mechanism of miR-142-5p in Parkinson’s disease (PD) are still ominous. METHODS: To simulate the PD, 6-hydroxydopamine (6-OHDA)-treated SH-SY5Y cell model was used in this study. Levels of messenger RNA and protein were tested by quantitative real-time polymerase chain reaction and Western blot analyses, respectively. The direct interaction between miR-142-5p and Beclin 1 (BECN1) was assessed by luciferase reporter assay. Furthermore, Cell Counting Kit-8 assay was performed to assess cytotoxicity of SH-SY5Y cell. RESULTS: In consequence, a significant decrease of miR-142-5p was observed in 6-OHDA-induced SH-SY5Y cells. Over-/Low-expressed miR-142-5p resulted in a significant enhancement/inhibition on cell vitalities of 6-OHDA-treated SH-SY5Y cells, which might be modulated by repressing cellular autophagy through inhibiting level of BECN1 and LC3 II/LC3 I and elevating P62 level. Luciferase reporter assay showed that the BECN1 was the target gene of miR-142-5p. Additionally, the loss/gain of BECN1 rescued/blocked the effects of miR-142-5p on the viability of 6-OHDA-induced SH-SY5Y cells. CONCLUSIONS: These results highlight that miR-142-5p functions as a neuroprotective regulator in 6-OHDA-induced neuronal SH-SY5Y cells simulating PD model in vitro via regulating autophagy-related protein BECN1 and autophagy to influence cell viability.