Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, 130021, China.
Clin Transl Oncol. 2022 Nov;24(11):2045-2054. doi: 10.1007/s12094-022-02863-2. Epub 2022 Jul 27.
The somatic mutation of liver kinase B1 (LKB1) has been implicated in various tumors, which is reflected in the survival, proliferation, and metastasis of tumor cells. However, the regulation of LKB1 in lipid metabolism, a process that is involved in tumor progression is not completely clear. We conclude that LKB1 deficiency results in abnormal expression and activation of multiple molecules related to lipid metabolism which locate downstream of AMP-activated protein kinase (AMPK) or salt-induced kinase (SIK). Abnormal lipid metabolism induced by LKB1 deficiency contributes to the proliferation and metastasis of tumor cells through energy regulation.
肝激酶 B1（LKB1）的体细胞突变与各种肿瘤有关，这反映在肿瘤细胞的存活、增殖和转移中。然而，LKB1 在脂质代谢中的调节作用，这一过程涉及肿瘤的进展还不完全清楚。我们得出结论，LKB1 的缺乏导致与脂质代谢相关的多种分子的异常表达和激活，这些分子位于 AMP 激活的蛋白激酶（AMPK）或盐诱导激酶（SIK）的下游。LKB1 缺乏引起的异常脂质代谢通过能量调节促进肿瘤细胞的增殖和转移。
