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
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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
“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 ResearchVol. 11, Issue 6, Pages: 818-838(2024)
Affiliations:
Key Laboratory of Hepatobiliary and Pancreatic Surgery, Institute of Hepatobiliary Surgery, Southwest Hospital, Army Medical University, Chongqing 400038, China
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:
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.
Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice