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. Author manuscript; available in PMC: 2019 Aug 16.
Published in final edited form as: Gut. 2018 Oct 18;68(7):1271–1286. doi: 10.1136/gutjnl-2017-315690

Figure 7. Schematic depiction of KMT2D transcriptional regulation and downstream mechanistic targets and pathways in pancreatic cancer.

Figure 7.

Methylation of 2 single CpG sites transcriptionally represses KMT2D histone methyltransferase expression. Suppression of KMT2D induces aerobic glycolysis and lipid levels in pancreatic cancer. SLC2A3 consists a key mediator of the cellular growth and metabolic effects triggered by KMT2D downregulation. Docosadienoic, docosatrienoic and docosatetraenoic acid represent the top KMT2D-regulated FAs and harbor oncogenic properties in pancreatic cancer cells.