Research Papers:

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

Jung-Hyun Cho _, Ho-Young Chun, Jung Suk Lee, Jee-Hyun Lee, Kyu Jin Cheong, Youn-Sang Jung, Tae-Gyun Woo, Min-Ho Yoon, Ah-Young Oh, So-Mi Kang, Chunghui Lee, Hokeun Sun, Jihwan Hwang, Gyu-Yong Song and Bum-Joon Park

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Oncotarget. 2016; 7:35144-35158. https://doi.org/10.18632/oncotarget.9059

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Jung-Hyun Cho1,*, Ho-Young Chun1,*, Jung Suk Lee2,*, Jee-Hyun Lee2, Kyu Jin Cheong2, Youn-Sang Jung1, Tae-Gyun Woo1, Min-Ho Yoon1, Ah-Young Oh1, So-Mi Kang1, Chunghui Lee3, Hokeun Sun3, Jihwan Hwang4, Gyu-Yong Song2, Bum-Joon Park1

1Department of Molecular Biology, College of Natural Science, Pusan National University, Busan, Korea

2College of Pharmacy, Chungnam National University, Daejoen, Korea

3Department of Statistics, College of Natural Science, Pusan National University, Busan, Korea

4Department 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: [email protected]

Gyu-Yong Song, e-mail: [email protected]

Keywords: stress hormone, MTOC, cancer prevention

Received: October 06, 2015    Accepted: April 11, 2016    Published: April 27, 2016


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.

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