Endothelial fatty liver binding protein 4: a new targetable mediator in hepatocellular carcinoma related to metabolic syndrome.

This original study demonstrates that liver sinusoidal endothelial cells (LSECs) exposed to conditions mimicking NAFLD -namely high concentrations of glucose, insulin, or VEGFA- release FABP4. They also observed that fatty...
PUBLISHED IN: Oncogene. 2019 Apr;38(16):3033-3046.

Authors : Laouirem S, Sannier A, Norkowski E, Cauchy F, Doblas S, Rautou PE, Albuquerque M, Garteiser P, Sognigbé L, Raffenne J, van Beers BE, Soubrane O, Bedossa P, Cros J, Paradis V.

Commentary

This original study demonstrates that liver sinusoidal endothelial cells (LSECs) exposed to conditions mimicking NAFLD -namely high concentrations of glucose, insulin, or VEGFA- release FABP4. They also observed that fatty acid-binding protein 4 (FABP4) released by LSECs, partly in microvesicles, exerts pro-oncogenic effects, since it induces hepatocyte proliferation. In mice fed a high-fat diet, specific inhibition of FABP4 reduces hepatocellular carcinoma growth. In conclusion, this study demonstrates the emerging oncogenic role of liver endothelial cells through FABP4 in hepatocellular carcinoma related to metabolic syndrome.

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Dr. G. Bozet, MD

Dr. G. Bozet, MD

Articles: 174

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