title: Rhus verniciflua extract modulates survival of MCF-7 breast cancer cells through the modulation of AMPK-pathway.
abstract: Rhus verniciflua STOKES (RVS) is used as an anti-cancer agent in traditional herbal medicine. However, the underlying molecular mechanism of its action is poorly understood. Here, we elucidated the mechanism of the anti-cancer mechanism of RVS in MCF-7 human breast cancer cells. We found that RVS increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed cell viability in an AMPK-dependent fashion. RVS also induced an increase in reactive oxygen species (ROS) levels. RVS-induced AMPK phosphorylation was not observed in the presence of N-acetyl-cysteine (NAC), which indicated that ROS is associated with RVS-induced AMPK phosphorylation. In addition, fluorescent staining (Annexin V/propidium iodide) revealed that RVS increased the expression of Annexin V, which indicates that RVS leads to cancer-induced apoptosis. Moreover, RVS increased the phosphorylation of p53 and the expression of Bax. The inhibition of AMPK blocked RVS-induced p53 phosphorylation and Bax expression, which suggests that AMPK is involved in RVS-induced cancer apoptosis. Taken together, these results demonstrate that RVS has anti-tumor effects on MCF-7 cells through an AMPK-signaling pathway.
authors.affiliation: Institute of Human Genetics, Department of Anatomy, Korea University College of Medicine.
authors.forename: Jung Ok
authors.initials: JO
authors.lastname: Lee
authors.forename: Ji Wook
authors.initials: JW
authors.lastname: Moon
authors.forename: Soo Kyung
authors.initials: SK
authors.lastname: Lee
authors.forename: So Mi
authors.initials: SM
authors.lastname: Kim
authors.forename: Nami
authors.initials: N
authors.lastname: Kim
authors.forename: Seong-Gyu
authors.initials: SG
authors.lastname: Ko
authors.forename: Hyeon Soo
authors.initials: HS
authors.lastname: Kim
authors.forename: Sun Hwa
authors.initials: SH
authors.lastname: Park
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism*; D000111:Acetylcysteine / Q000494:pharmacology; D017304:Annexin A5 / Q000096:biosynthesis; D000970:Antineoplastic Agents / Q000737:chemistry / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology*; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D061986:MCF-7 Cells; D010766:Phosphorylation / Q000187:drug effects; D024301:Plant Bark / Q000737:chemistry*; D010936:Plant Extracts / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D029045:Rhus / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis
chemical_list: D017304:Annexin A5; D000970:Antineoplastic Agents; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase; D000111:Acetylcysteine