Fig 2: AP-1 control of the SQSTM1 promoter in stromal cells is critical for PCa tumor growth and invasion(A and B) qPCR of mRNA levels of the indicated genes in WPMY-1 cells treated or not with lactate (A) and NAD+ (B) for 48 h (n = 3 biological replicates).(C) GSEA of “LACTATE UP” and “LACTATE DOWN” gene signatures in CAFs versus NAFs gene set GEO: GSE34312.(D) qPCR of mRNA levels of indicated genes in sgC and sgAP-1A WPMY-1 cells (n = 3 biological replicates).(E–G) Experimental design (E), migration (F), and invasion (G) of PC3 cells co-cultured with sgC or sgAP-1A WPMY-1 cells for 16 h. Representative images and quantification (n = 3 biological replicates). Scale bars: 50 µm.(H and I) Experimental design (H) and H&E staining (I) of organotypic gels combining PC3 cells with sgC and sgAP-1A WPMY-1 cells. Quantification of PC3 cells invasion and proliferation of experiments shown in (I) (n = 3 biological replicates). Scale bars: 100 µm.(J–M) Subcutaneous xenograft co-implantation in castrated NSG mice (male, 7 weeks old) of PC3 PCa cells with sgC or sgAP-1A WPMY-1 cells (PC3 + sgC WPMY-1: n = 8; PC3 + sgAP-1A WPMY-1: n = 8). Experimental design (J); tumor weight (K); gross images (L); and immunohistochemistry (IHC) for Masson’s trichrome, HA, and aSMA (M). Scale bars: 1 cm (L); 50 µm (M).Results are shown as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. See also Figure S5.

Fig 3: OSA patients exhibit increased hepatic steatosis and elevated levels of hepatic proteins associated with autophagy, ER stress, and lipogenesis. (A) H&E staining of liver tissue samples from patients with and without OSA (Scale bars: 100 and 50 μM). (B) Hepatic FASn, p62, LC3A/B, and p-EIF2α/EIF2α levels were measured in patients with and without OSA. (C) Quantification of SCD1, FASn, P62 with β-Actin and LC3B/A protein levels serving as a loading control. In addition, the p-EIF2α/EIF2α ratio was compared in individuals with and without OSA (*p < 0.05).

Fig 4: CQ can promote apoptosis in ARHI-glioma cells. a-b Cell viability of LN229 and T98G cells transfected with ARHI and negative control plasmids cultured with 2 mM 3-MA or 3 μM CQ after 48 h. c-d Western blot showing SQSTM1, LC3, Bcl2, Ras and ARHI levels in LN229 cells after treatment with 2 mM 3-MA or 3 μM CQ for 48 h. The experiments were repeated 3 times independently. e-h After treatment with 3-MA or CQ, LN229 cells were analyzed by flow cytometry and examined by western blot for apoptosis-related caspase-3 protein. All experiments were repeated 3 times independently

Fig 5: Poly-arginine R18 treatment induces neurocyte cell autophagy in TBI rats. Quantification of (A) LC3-1 and LC3-2, (B) Beclin-1, (C) p62 and (D) Bax protein expression and (E) western blot analysis. ##P<0.01 vs. the control group; **P<0.01 vs. the model group. TBI, traumatic brain injury; Bax, Bcl-2 associated X; model, traumatic brain injury rats; R18, poly-arginine R18 treated rats.