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Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice
RESEARCH | Updated:2025-12-13
    • Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

    • In the field of liver cancer research, this study investigates how FBXL6 regulates KRAS and KRASG12D activity in hepatocellular carcinoma. Expert established the FBXL6/KRAS/ERK/mTOR/PRELID2/ROS axis, which provides a potential therapeutic strategy to treat aggressive liver cancer.
    • Military Medical Research   Vol. 11, Issue 6, Pages: 818-838(2024)
    • DOI:10.1186/s40779-023-00501-8    

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    • Published:2024-12

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  • Cite this article as: Xiong HJ, Yu HQ, Zhang J, Fang L, Wu D, Lin XT, et al. Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice. Mil Med Res. 2023;10(1):68. DOI: 10.1186/s40779-023-00501-8.

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