Biomol Ther  
Gomisin G Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing AKT Phosphorylation and Decreasing Cyclin D1
Sony Maharjan1,†, Byoung Kwon Park1,†, Su In Lee1, Yoonho Lim2, Keunwook Lee3 and Hyung-Joo Kwon1,4,*
1Center for Medical Science Research, College of Medicine, Hallym University, Chuncheon 24252,
2Division of Bioscience and Biotechnology, BMIC, Konkuk University, Seoul 05029,
3Department of Biomedical Science, College of Natural Science, Hallym University, Chuncheon 24252,
4Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Republic of Korea
E-mail: hjookwon@hallym.ac.kr
Tel: +82-33-248-2635, Fax: +82-33-241-3640
The first two authors contributed equally to this work.
Received: November 30, 2017; Revised: January 5, 2018; Accepted: January 9, 2018; Published online: March 28, 2018.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
A type of breast cancer with a defect in three molecular markers such as the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor is called triple-negative breast cancer (TNBC). Many patients with TNBC have a lower survival rate than patients with other types due to a poor prognosis. In this study, we confirmed the anti-cancer effect of a natural compound, Gomisin G, in TNBC cancer cells. Treatment with Gomisin G suppressed the viability of two TNBC cell lines, MDA-MB-231 and MDA-MB-468 but not non-TNBC cell lines such as MCF-7, T47D, and ZR75-1. To investigate the molecular mechanism of this activity, we examined the signal transduction pathways after treatment with Gomisin G in MDA-MB-231 cells. Gomisin G did not induce apoptosis but drastically inhibited AKT phosphorylation and reduced the amount of retinoblastoma tumor suppressor protein (Rb) and phosphorylated Rb. Gomisin G induced in a proteasome-dependent manner a decrease in Cyclin D1. Consequently, Gomisin G causes cell cycle arrest in the G1 phase. In contrast, there was no significant change in T47D cells except for a mild decrease in AKT phosphorylation. These results show that Gomisin G has an anti-cancer activity by suppressing proliferation rather than inducing apoptosis in TNBC cells. Our study suggests that Gomisin G could be used as a therapeutic agent in the treatment of TNBC patients.
Keywords: AKT, Cell cycle, Cell proliferation, Cyclin D1, Gomisin G, Triple negative breast cancer


This Article


Cited By Articles
  • CrossRef (0)

e-submission

Archives