Objective To investigate the effects of LncRNA SNHG1 targeting miR-140-5p on the proliferation, apoptosis and autophagy of rheumatoid arthritis (RA) fibroblasts.

Methods The rheumatoid arthritis fibroblasts were cultured and passaged to obtain cells in the logarithmic growth phase, and those were seeded in 96-well plates at 5.0 × 10⁴ cells/well. The above cells were divided into the SNHG1 down-regulated group, SNHG1 up-regulated group, SNHG1 control group, miR-140-5p down-regulated group, miR-140-5p up-regulated group, miR control group, pcDNA-SNHG1 + miR-NC group and pcDNA-SNHG1 + miR-140-5p group, and the untransfected cells were set as the control group, with 6 replicate wells in each group. After 48 hours of transfection, the transfection efficiency of the cells in each group was detected. The cell proliferation ability was detected by the cell counting kit 8 (CCK-8) experiment. The apoptosis rate of the cells was detected by flow cytometry. The RT-qPCR was used to the detect the mRNA expression levels of miR-140-5p expression and B-cell lymphoma-2 (Bcl-2), Bcl-2-related X (Bax), LC3-Ⅰ and LC3-Ⅱ. The protein expression levels of Bcl-2, Bax, LC3-Ⅰ and LC3-Ⅱ were detected by western blotting. The dual-luciferase reporter gene assay and RNA co-immunoprecipitation (RIP) assay were used to verify the targeted regulation of miR-140-5p by SNHG1.

Results Compared with the control group and SNHG1 control group, the cell proliferation ability increased, and the apoptosis rate decreased in the up-regulated SNHG1 group (P ＜ 0.05). Compared with the control group and miR control group, the cell proliferation ability and apoptosis rate in the Mir-140-5p up-regulated group decreased and increased, respectviely (P ＜ 0.05). Compared with the pcDNA-SNHG1 + miR-NC group, the cell proliferation ability and apoptosis rate in pcDNA-SNHG1 + miR-140-5p group decreased and increased respectviely (P ＜ 0.05). Compared with the control group and SNHG1 control group, the mRNA and protein expression levels of miR-140-5p and Bax decreased, while the mRNA and protein expression levels of Bcl-2, LC3-Ⅰ and LC3-Ⅱincreased in the up-regulated SNHG1 group (P ＜ 0.05). Compared with the control group and miR control group, the mRNA and protein expression levels of Mir-140-5p and Bax increased, while the mRNA and protein expression levels of Bcl-2, LC3-Ⅰ and LC3-Ⅱ decreased in the up-regulated Mir-136-5P group (P ＜ 0.05). Compared with the pcDNA-SNHG1 + miR-NC group, the mRNA and protein expression levels of miR-140-5p and Bax increased, while the mRNA and protein expression levels of Bcl-2, LC3-Ⅰ and LC3-Ⅱ decreased in pcDNA-SNHG1 + miR-140-5p group (P ＜ 0.05). The results of Dual luciferase reporter gene assay and RIP assay confirmed that the SNHG1 targeted the miR-140-5p.

Conclusions The SNHG1 can improve the proliferation and autophagy capacity of RA fibroblasts, inhibit their apoptosis and promote the progression of RA, which may be achieved by targeted inhibition of the expression of miR-140-5p, promoting the expression of Bcl-2, LC3-Ⅰ, LC3-Ⅱ, and inhibiting the expression of Bax.