Fig. 8

CircRNF13 inhibits the proliferation and metastasis of NPC via SUMO2. A Overexpression of SUMO2 rescued the circRNF13 knockdown-mediated altered proliferative capacity of HNE2 and CNE2 cells, as assessed using MTT assay. Data have been represented as mean ± SD. **, p < 0.01; ***, p < 0.001. B Overexpression of SUMO2 decreased the circRNF13 knockdown-mediated altered migration of HNE2 and CNE2 cells, as assessed using wound-healing assays. All experiments were repeated at least three times (Scale bar: 100 μm). Data have been represented as mean ± SD; ns, no significance; ***, p < 0.001. C. Overexpression of SUMO2 reduced the circRNF13 knockdown-mediated altered invasive ability of HNE2 and CNE2 cells, as assessed using Transwell assays. All experiments were repeated at least three times (Scale bar: 100 μm). Data have been represented as mean ± SD; ns, no significance; ***, p < 0.001. D The extracellular acidification rate (ECAR) was measured using Seahorse XF assay in HNE2 and CNE2 cells co-transfected with sicircRNF13 and SUMO2 overexpression vector. Glycolysis, glycolytic capacity, and glycolytic reserve were analyzed. All experiments were repeated at least three times. Data have been represented as mean ± SD; ns, not significant; **, p < 0.01. E Representative images of SUMO2 and GLUT1 expression in lung tissues of nude mice, as determined using immunohistochemistry (n = 7 per group, 200 × , scale bar: 50 μm). F Schematic diagram of the molecular mechanism of circRNF13 in NPC. circRNF13 may activate and stabilize the SUMO2 protein by binding to the 3′-UTR of SUMO2 mRNA. Upregulation of SUMO2 promotes GLUT1 degradation through SUMOylation and ubiquitination of GLUT1, which regulates the AMPK pathway by inhibiting glycolysis, ultimately resulting in the proliferation and metastasis of NPC