Open AccessTubeimoside I induces autophagy in HepG2 cells by activating the AMP‑activated protein kinase signaling pathway
Author(s) -
Ruan Cheng-xu,
Lijuan You,
Yingdong Qiu,
Xiao Cui,
Defeng Wu
Publication year - 2020
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2020.11604
Subject(s) - autophagy , ampk , cell cycle , microbiology and biotechnology , protein kinase a , apoptosis , signal transduction , biology , cancer cell , phosphorylation , cancer research , oncogene , kinase , cell , cell growth , chemistry , cancer , biochemistry , genetics
Tubeimoside I (TBMS) is a natural compound with antitumor properties. However, the detailed mechanism underlying the function of TBMS in liver cancer has not been fully elucidated. In the present study, TBMS was shown to suppress cell proliferation and induce S phase cell cycle arrest in HepG2 cells. Furthermore, TBMS treatment induced autophagy, evidenced by autophagosome accumulation, and increased the mRNA expression of Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3)-I. However, flow cytometry analysis demonstrated that TBMS exerted no effect on cell apoptosis. Moreover, TBMS increased the phosphorylation of AMP-activated protein kinase (AMPK) in a concentration-dependent manner, thereby activating the AMPK signaling pathway. A specific AMPK inhibitor, compound C (CC), caused markedly suppressed TBMS-induced accumulation of LC3-II. In addition, the mRNA expression of LC3-I and Beclin 1 was also suppressed in cells treated with TBMS and CC in combination. The results of the present study provide new insights into the role of TBMS in inducing autophagy and support the potential application of TBMS for liver cancer treatment in the clinical setting.