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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the death of upper and lower motor neurons. MicroRNAs (miRNAs) are reported to be closely related to the development of ALS. However, the precise functions of miRNAs in the pathogenesis of ALS remain largely unknown. In previous studies, we determined that  miRNA-193b-3p  was significantly downregulated in patients with sporadic ALS (sALS). Here, we observed that  miRNA-193b-3p  was downregulated in the SOD1 G93A  mouse model of ALS and promoted cell death in NSC-34 cells. We further found that  miR-193b-3p  directly targeted tuberous sclerosis 1 (TSC1) to regulate mechanistic target of rapamycin complex 1 (mTORC1) activity. Downregulation of  miR-193b-3p  led to TSC1 increase accompanied with mTORC1 inactivation, and  vice versa . Moreover, downregulation of  miR-193b-3p  promoted protective autophagy and cell survival in NSC-34 cells. In contrast, upregulation of  miR-193b-3p  activated mTORC1 signaling, leading to inhibition of autophagy and promotion of cell death. Taken together, our study suggests that downregulation of  miR-193b-3p  is required for cell survival by targeting TSC1/mTOR signaling in NSC-34 cells and provides a novel target for improving the clinical therapy of ALS.

Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells