Elevated FBXL6 activates both wild-type KRAS and mutant KRAS<sup>G12D</sup> and drives HCC tumorigenesis <italic style="font-style: italic">via</italic> the ERK/mTOR/PRELID2/ROS axis in mice

Hao-Jun Xiong; Hong-Qiang Yu; Jie Zhang; Lei Fang; Di Wu; Xiao-Tong Lin; Chuan-Ming Xie

doi:10.1186/s40779-023-00501-8

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Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D 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 KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice
- Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice
- “在癌症研究领域，本研究探讨了FBXL6如何调节肝细胞癌中的KRAS和KRASG12D活性。专家建立了FBXL6/KRAS/ERK/mTOR/PREDLID2/ROS轴，为治疗侵袭性肝癌提供了一种潜在的治疗策略。”
- MMR 2024年11卷第6期页码：818-838
- Affiliations：
  
  Key Laboratory of Hepatobiliary and Pancreatic Surgery, Institute of Hepatobiliary Surgery, Southwest Hospital, Army Medical University, Chongqing 400038, China
- Author bio：
  
  *cmxie@tmmu.edu.cn
- Funds：
  
  the National Natural Science Foundation of China(82370631);the Talent Foundations from Army Medical University(4174C6);the Chongqing Government(CQYC20220303727);the National Natural Science Foundation of China(31900449)
- DOI：10.1186/s40779-023-00501-8
  中图分类号：
- 纸质出版：2024-12
- Accepted：
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Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice[J]. MMR, 2024,11(6):818-838.

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 KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice. Mil Med Res. 2023;10(1):68.
Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice[J]. MMR, 2024,11(6):818-838. DOI： 10.1186/s40779-023-00501-8.

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 KRAS^G12D 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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Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

DOI：10.1186/s40779-023-00501-8

Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

Elevated FBXL6 activates both wild-type KRAS and mutant KRAS^G12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice