Fig. 4 | Nature Communications

Fig. 4

From: An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma

Fig. 4

CCRK activates mTORC1 signaling through GSK3β/TSC2 cascade. a Ectopic CCRK expression in LO2 and CCRK KO Huh7 cells activates mTORC1 signaling, which was abrogated by suppression of GSK3β phosphorylation at Ser9 (p-GSK3βSer9) via over-expression of the constitutively-active S9A-GSK3β mutant. Western blot analysis was used to detect the protein expression of mTORC1 downstream molecules. b Knockdown of CCRK in HepG2 and Huh7 cells impaired the activation of mTORC1 signaling, which was rescued by the silencing of TSC2. c, d Dietary obesity-induced CCRK expression is responsible for the activation of mTORC1 signaling cascades in both c NASH and d NASH-HCC models, and such CCRK-dependent effects were abolished following knockdown of Ccrk. The establishment of NASH and NASH-HCC models are as described in Figs. 1a and 2a

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