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Comment
. 2024 Jun 6;73(7):1046-1048.
doi: 10.1136/gutjnl-2023-331857.

High-fat diet-induced AKT-palmitoylation in hepatocellular carcinoma: a breakthrough mechanistic investigation

Claudia R Keating  1 , Diego F Calvisi  2 , Wei Qiu  3
Affiliations
Comment

High-fat diet-induced AKT-palmitoylation in hepatocellular carcinoma: a breakthrough mechanistic investigation

Claudia R Keating et al. Gut. .
No abstract available

Keywords: HEPATOCELLULAR CARCINOMA.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1:
Figure 1:. Description of PA-ZDHHC-AKT axis in MASLD and HCC.
Palmitic acid (PA) ingested from HFD or produced endogenously by TCA and FASN has been shown to activate AKT. The conjugation of PA to AKT by ZDHH17/24 has been shown to promote the activation and oncogenicity of AKT, and lead to MASLD and HCC. Conversely, the depalmitolyation of AKT by APT2 has been shown to reduce the oncogenic function of AKT. Several points on this pathway can be exploited for therapeutic intervention, including but not limited to dietary restriction of PA, inhibition of PA production, and inhibition of PA conjugation. See Bu et al. for details [5]. Created with BioRender.com. PA, palmitic acid; HFD, high-fat diet; TCA, tricarboxcylic acid cycle; FASN, fatty acid synthase; ZDHHC17/24, zinc finger DHHC domain-containing protein 17 and 24; APT2, acyl-protein thioesterase 2; MASLD, metabolic dysfunction-associated steatohepatitis; HCC, hepatocellular carcinoma.
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