The role of liver kinase B1 in tumor progression through regulation of lipid metabolism

被引：1

作者：

Geng, Jialu ^{[1
]}

Zhang, Yanghe ^{[1
]}

Meng, Qingfei ^{[1
]}

Yan, Hang ^{[1
]}

Wang, Yishu ^{[1
]}

机构：

[1] Jilin Univ, Key Lab Pathobiol, Minist Educ, Changchun 130021, Peoples R China

来源：

CLINICAL & TRANSLATIONAL ONCOLOGY | 2022年 / 24卷 / 11期

基金：

中国国家自然科学基金;

关键词：

LKB1; Lipid metabolism; Tumor; AMPK; ACETYL-COA CARBOXYLASE; FATTY-ACID OXIDATION; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAY; LUNG-CANCER; LKB1; CELLS; ACCUMULATION; GLUCOSE;

D O I：

10.1007/s12094-022-02863-2

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：2045 / 2054

页数：10

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