Fig. 6: Proposed model on the role of TAK1 inhibition in KRAS-driven ADM and PDAC development. | Nature Communications

Fig. 6: Proposed model on the role of TAK1 inhibition in KRAS-driven ADM and PDAC development.

From: A decision point between transdifferentiation and programmed cell death priming controls KRAS-dependent pancreatic cancer development

Fig. 6: Proposed model on the role of TAK1 inhibition in KRAS-driven ADM and PDAC development.

KRAS-dependent, and likely KRAS-independent, ADM induction leads to upregulated expression of PCD mediating molecules. Through its NF-κB-independent prosurvival functions, TAK1 prevents elimination of the PCD-primed transdifferentiated ductal cells, thereby enabling PanIN formation and PDAC development. In contrast, TAK1 deficiency/inhibition impairs cell survival during ADM and prevents PanIN establishment and progression to PDAC73.

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