Open AccessApelin‐mediated deamidation of HMGA1 promotes tumorigenesis by enhancing SREBP1 activity and lipid synthesis
Author(s) -
Zhu Yihan,
Yang Ying,
Bu Hong,
Huang Hong,
Chen Hongyu,
Ran Jingjing,
Qin Liwen,
Ni Yinyun,
Yao Menglin,
Song Tingting,
Li Mufeng,
Yang Yongfeng,
Guo Tingting,
Chao Ningning,
Liu Zhiqing,
Li Weimin,
Zhang Li
Publication year - 2022
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.15515
Subject(s) - sterol regulatory element binding protein , deamidation , apelin , chemistry , carcinogenesis , cell growth , lipid metabolism , cancer cell , biochemistry , cancer research , microbiology and biotechnology , biology , receptor , cancer , sterol , cholesterol , enzyme , genetics , gene
Enhanced fatty acid synthesis provides proliferation and survival advantages for tumor cells. Apelin is an adipokine, which serves as a ligand of G protein–coupled receptors that promote tumor growth in malignant cancers. Here, we confirmed that apelin increased sterol regulatory element–binding protein 1 (SREBP1) activity and induced the expression of glutamine amidotransferase for deamidating high‐mobility group A 1 (HMGA1) to promote fatty acid synthesis and proliferation of lung cancer cells. This post‐translational modification stabilized the HMGA1 expression and enhanced the formation of the apelin‐HMGA1‐SREBP1 complex to facilitate SREBP1 activity for lipid metabolism and lung cancer cell growth. We uncovered the pivotal role of apelin‐mediated deamidation of HMGA1 in lipid metabolism and tumorigenesis of lung cancer cells.