Prevention effect of rare ginsenosides against stress-hormone induced MTOC amplification

// Jung-Hyun Cho 1, * , Ho-Young Chun 1, * , Jung Suk Lee 2, * , Jee-Hyun Lee 2 , Kyu Jin Cheong 2 , Youn-Sang Jung 1 , Tae-Gyun Woo 1 , Min-Ho Yoon 1 , Ah-Young Oh 1 , So-Mi Kang 1 , Chunghui Lee 3 , Hokeun Sun 3 , Jihwan Hwang 4 , Gyu-Yong Song 2 , Bum-Joon Park 1 1 Department of Molecular Biology, College of Natural Science, Pusan National University, Busan, Korea 2 College of Pharmacy, Chungnam National University, Daejoen, Korea 3 Department of Statistics, College of Natural Science, Pusan National University, Busan, Korea 4 Department of Microbiology, College of Natural Science, Pusan National University, Busan, Korea * These authors equally contribute at this work Correspondence to: Bum-Joon Park, e-mail: bjpark1219@pusan.ac.kr Gyu-Yong Song, e-mail: gysong@cnu.ac.kr Keywords: stress hormone, MTOC, cancer prevention Received: October 06, 2015     Accepted: April 11, 2016     Published: April 27, 2016 ABSTRACT Stress has been suggested as one of important cause of human cancer without molecular biological evidence. Thus, we test the effect of stress-related hormones on cell viability and mitotic fidelity. Similarly to estrogen, stress hormone cortisol and its relative cortisone increase microtubule organizing center (MTOC) number through elevated expression of γ-tubulin and provide the Taxol resistance to human cancer cell lines. However, these effects are achieved by glucocorticoid hormone receptor (GR) but not by estrogen receptor (ER). Since ginsenosides possess steroid-like structure, we hypothesized that it would block the stress or estrogen-induced MTOC amplification and Taxol resistance. Among tested chemicals, rare ginsenoside, CSH1 (Rg6) shows obvious effect on inhibition of MTOC amplification, γ-tubulin induction and Taxol resistance. Comparing to Fulvestant (FST), ER-α specific inhibitor, this chemical can block the cortisol/cortisone-induced MTOC deregulation as well as ER-α signaling. Our results suggest that stress hormone induced tumorigenesis would be achieved by MTOC amplification, and CSH1 would be useful for prevention of stress-hormone or steroid hormone-induced chromosomal instability.