Fig. 5: Metabolic reprogramming in HPV-KI is crucial for S100A8/A9 dysregulation. | Cell Death & Disease

Fig. 5: Metabolic reprogramming in HPV-KI is crucial for S100A8/A9 dysregulation.

From: Site-specific HPV18 integration facilitates cervical carcinogenesis through metabolic reprogramming-induced dysfunction of the SpHK1/S1P/S1PR1 pathway

Fig. 5

A Diagram illustrating 2-DG inhibits HK activity and interferes glycolysis. B Heatmap showing the up- and down-regulated genes of IL-17 signaling pathway in 2-DG-treated HPV-KI/HPV-KI. C Heatmap of the abundance of metabolites involved in glycolysis between HPV-KI and 2-DG-treated HPV-KI. D KEGG analysis reveals Lipid-omics changes between HPV-KI and 2-DG-treated HPV-KI based on the DA Score of the pathway, highlighting annotations for sphingolipid metabolism pathway in red bold. E The diagram depicts the de novo synthesis of GL facilitated by DHAP, wherein SpHK1 is activated by PA to enhance S1P secretion. The process is disrupted by inhibition of GPAT by FSG67. F Heatmap illustrates up- and down-regulated genes involved in the IL-17 signaling pathway in FSG67- treated HPV-KI/HPV-KI cells. G S100A8/A9 protein expression in 2-DG-treated, FSG67-treated and untreated HPV-KI cells. H Western blot analysis of ERK1/2, IκBα, phosphorylated ERK1/2, and phosphorylated IκBα protein levels in untreated, 2-DG-treated and FSG67-treated HPV-KI cells. The data are calculated by two-tailed Student’s t-test. P value is denoted as *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001, “ns” represents “not significant”. I Expression of S100A8/A9 in 2-DG-treated and FSG67-treated HPV-KI cells replenished with Gro3P and LPA.

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