Fig 2: NEAT1 regulates the MEST/ATGL axis by regulating let-7 g. A The binding site of let-7 g and MEST predicted using starBase. B MEST expression in ovarian cancer samples in the TCGA database. C The binding of let-7 g to MEST verified by dual luciferase reporter gene assay. *p < 0.05 vs. the NC-mimic group. D Co-expression analysis of MEST and ATGL expression in ovarian cancer samples within the TCGA database. The x-axis represents the expression of MEST, and the y-axis represents the expression of ATGL. E The expression of let-7 g, MEST and ATGL in HO8910 and SKOV3 cells after silencing of let-7 g determined by RT-qPCR. F The protein expression of MEST and ATGL in HO8910 and SKOV3 cells after silencing of let-7 g determined by western blot analysis. G The expression levels of MEST and ATGL in HO8910 and SKOV3 cells after silencing NEAT1, as determined by RT-qPCR. H The protein expression of MEST and ATGL in HO8910 and SKOV3 cells after silencing NEAT1 determined by western blot analysis. I MEST expression in ovarian cancer tissues and adjacent normal tissues determined by RT-qPCR, n = 68. J, ATGL expression in ovarian cancer tissues and adjacent normal tissues determined by RT-qPCR, n = 68. K Positive expression of MEST and ATGL proteins in ovarian cancer tissues and adjacent normal tissues determined by immunohistochemistry. L Pearson correlation analysis of let-7 g expression with MEST expression in clinical samples, n = 68. In figure D, E *p < 0.05 vs. the NC-mimic group. #p < 0.05 vs. the NC-inhibitor group. In figure F, G *p < 0.05 vs. the oe-NC group. #p < 0.05 vs. the si-NC group. In figure H, I *p < 0.05 vs. adjacent normal tissues. The measurement data were expressed as mean ± standard deviation. Comparisons between two groups were conducted by t-test, while comparisons among multiple groups were assessed by one-way ANOVA followed by Tukey's post hoc test. All cell experiments were performed 3 times independently

Fig 3: Silencing of NEAT1 restrains in vivo tumorigenesis by regulating the let-7 g/MEST/ATGL axis. Mice were treated with sh-NEAT1, let-7 g inhibitor or both. A The expression levels of NEAT1, let-7 g, MEST and ATGL in tumor tissues determined by RT-qPCR. B The protein expression of MEST and ATGL in tumor tissues determined by western blot analysis. C The positive expression of MEST and ATGL proteins in tumor tissues by immunohistochemistry (400 ×). D Representative images of tumors obtained after 40 d of tumor xenograft in nude mice. E Tumor growth curve. F The final tumor weight in each group. G Cell apoptosis of tumor tissues quantified by TUNEL staining (400 ×). *p < 0.05 vs. the si-NC + NC-inhibitor group. #p < 0.05 vs. the si-NEAT1 + NC-inhibitor group. Measurement data were depicted as mean ± standard deviation, and assessed by one-way ANOVA followed by Tukey's post hoc test. The data of each group at different time points were compared using repeated measures ANOVA followed by Bonferroni post hoc test

Fig 4: Schematic diagram depicting the mechanism by which NEAT1 is involved in ovarian cancer. NEAT1 competitively binds to let-7 g and inhibits its expression, thereby promoting MEST expression and inhibiting ATGL expression, and ultimately promoting the growth, migration, and invasion of ovarian cancer cells as well as tumor metastasis

Fig 5: P2X7R regulates the Wnt/ß-catenin pathway. (A) Protein and (B) mRNA levels of Wnt3a in 3T3-L1 cells following siRNA-wnt3a-1 or siRNA-wnt3a-2 transfection. (C) Protein and (D) mRNA levels of Wnt3a in 3T3-L1 cells following co-transfection of siRNA-P2XR-1 with siRNA-wnt3a-1 or siRNA-wnt3a-2. (E) mRNA and (F) protein expression levels of PPAR?, C/EBPa and FABP4. (G) Protein expression levels of ATGL, p-HSL and MGL. Data are presented as the mean ± standard deviation. **P<0.01, ***P<0.001. P2X7R, purinergic receptor P2X ligand-gated ion channel 7; siRNA small interfering RNA; NC, negative control; C/EBPa, CCAAT-enhancer-binding protein a; ATGL, adipose triglyceride lipase; p-HSL, phosphorylated hormone-sensitive lipase; MGL, monoacylglycerol lipase; PPAR?, peroxisome proliferator-activated receptor ?; FABP4, fatty acid binding protein 4.