Fig 2: MIR155-3p overexpression enhances hypoxia-induced autophagy and resists the effects of IL6 inhibition on human glioma cells. (A) MIR155-3p mimic promoted GFP-LC3B translocation. pSELECT-GFP-LC3B and MIR155-3p mimic-co-transfected U251 cells treated with the IL6 antibody (1 μg/ml) and siRNAs (Si IL6 321) for 24 h. Scale bar: 50 μm. Quantitative analysis of GFP-LC3B puncta is shown in the right panel. The data shown are the mean ± s.d. of 4 independent experiments. *, # and $, P < 0.01; **, P < 0.001; ***, P < 0.0001; one-way ANOVA. (B) The MIR155-3p mimic induced LC3B conversion and STAT3 activation in U251 and T98G cells. LC3B, SQSTM1, STAT3 and p-STAT3 levels were examined by western blot analysis. GAPDH served as the loading control.

Fig 3: Risperidone represses differentiation and autophagy while enhancing apoptosis via the TNF-α/SATB2 axis in vivo. A, Western blot analysis of differentiation-related proteins (OPG, collagen I and RANKL) expression in femur tissues of mice. The band intensity was assessed. B, statistical results of alizarin red S staining in femur tissues of mice. C, Western blot analysis of apoptosis-related proteins (cleaved PARP1, cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9) in femur tissues of mice. The protein band was assessed. D, apoptosis rate in femur tissues in mice assessed by TUNEL staining. E, representative images of femur tissues in mice stained by immunohistochemistry and statistical results of LC3B positive rate. F, Western blot analysis of autophagy-related proteins (LC3 II/I, Beclin1, and p62) in femur tissues of mice. The band intensity was quantified and analyzed. *p < 0.05, compared with mice introduced with lentivirus expressing si-NC. #p < 0.05, compared with mice introduced with Risperidone + lentivirus expressing si-NC. &p < 0.05, compared with mice introduced with Risperidone + lentivirus expressing si-TNF-α. The experiments are repeated 3 times n = 6

Fig 4: The role of TRIM14 overexpression in HCC cell cisplatin resistance and autophagy. (A,B) qRT-PCR and Western blot verified TRIM14 expression in cisplatin-resistant HCC cells (DDP-R). DDP at different concentrations (0, 0.5, 1, 2, 4, 8, and 16 μM) was applied to treat HCC cells that were transfected along with vector or TRIM14 overexpression plasmids. (C,D) CCK8 assay was used to evaluate the viability of HCC cells. (E–G) Western blot revealed the profiles of autophagy-correlated proteins (including LC3B, Beclin1, and p62). (H) The cells were treated with cisplatin (5 μM). Immunofluorescence was used to detect LC3B (green color) expression in the cells. Scale bars = 20 μm. The blue color shows DAPI. * p < 0.05, ** p < 0.01 and *** p < 0.001 (vs. the vector group). N = 3.

Fig 5: Lipid metabolism and pathological changes in pancreatic islets. (A) Index analysis of lipid metabolism (triglycerides, cholesterin, LDL, and HDL); (B) Immunological staining of p27, CD45, and cleaved-caspase3 in pancreatic islets; (C) Immunological staining of insulin and LC3B in pancreatic islets. NS, no statistic significance.