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

被引：15

作者：

Cho, Jung-Hyun ^{[1
]}

Chun, Ho-Young ^{[1
]}

Lee, Jung Suk ^{[2
]}

Lee, Jee-Hyun ^{[2
]}

Cheong, Kyu Jin ^{[2
]}

Jung, Youn-Sang ^{[1
]}

Woo, Tae-Gyun ^{[1
]}

Yoon, Min-Ho ^{[1
]}

Oh, Ah-Young ^{[1
]}

Kang, So-Mi ^{[1
]}

Lee, Chunghui ^{[3
]}

Sun, Hokeun ^{[3
]}

Hwang, Jihwan ^{[4
]}

Song, Gyu-Yong ^{[2
]}

Park, Bum-Joon ^{[1
]}

机构：

[1] Pusan Natl Univ, Coll Nat Sci, Dept Mol Biol, Busan, South Korea

[2] Chungnam Natl Univ, Coll Pharm, Daejoen, South Korea

[3] Pusan Natl Univ, Coll Nat Sci, Dept Stat, Busan, South Korea

[4] Pusan Natl Univ, Coll Nat Sci, Dept Microbiol, Busan, South Korea

来源：

ONCOTARGET | 2016年 / 7卷 / 23期

基金：

新加坡国家研究基金会;

关键词：

stress hormone; MTOC; cancer prevention; GLUCOCORTICOID-RECEPTOR; CANCER INCIDENCE; SERUM CORTISOL; IN-VITRO; PACLITAXEL; FULVESTRANT; KETOCONAZOLE; INSTABILITY; ANTAGONISTS; RESISTANCE;

D O I：

10.18632/oncotarget.9059

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.-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, gamma-tubulin induction and Taxol resistance. Comparing to Fulvestant (FST), ER-alpha specific inhibitor, this chemical can block the cortisol/cortisone-induced MTOC deregulation as well as ER-alpha 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.

引用

页码：35144 / 35158

页数：15

共 43 条

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