Open AccessA new meroterpenoid functions as an anti-tumor agent in hepatoma cells by downregulating mTOR activation and inhibiting EMT
Author(s) -
HL Wan,
Jiemei Li,
Keda Zhang,
Xiaoting Zou,
Lanlan Ge,
Fuqiang Zhu,
Haoran Zhou,
Minna Gong,
Tianwa Wang,
Chen Dongling,
Shusong Peng,
Boping Zhou,
Xiaobin Zeng
Publication year - 2018
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-018-31409-2
Subject(s) - apoptosis , pi3k/akt/mtor pathway , reprogramming , cancer research , epithelial–mesenchymal transition , cancer cell , chemistry , microbiology and biotechnology , mesenchymal stem cell , cell growth , programmed cell death , cell , cancer , biology , transition (genetics) , gene , biochemistry , genetics
Liver cancer, also known as primary liver cancer, is cancer that starts in the liver. JNU-144, a new meroterpenoid purified from Lithospermum erythrorhizon , has exhibited promising anticancer activity; however, the molecular mechanisms of action of JNU-144 on malignant cells remain unclear. Our studies revealed that JNU-144 suppressed cell viability and proliferation in hepatoma cells by downregulating mTOR activation. Meanwhile, JNU-144 activated the intrinsic apoptosis pathway and subsequently triggered apoptotic cell death in SMMC-7721 cells. We also found that JNU-144 inhibited the epithelial–mesenchymal transition in both SMMC-7721 and HepG2 cells through reprogramming of epithelial–mesenchymal transition (EMT)-related gene expression or regulating protein instability. These findings indicate that JNU-144 exerts potent anticancer activity in hepatoma cells and may be developed as a potential therapeutic drug.