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Evodiamine selectively targets cancer stem-like cells through the p53-p21-Rb pathway

Authors
Han, SeulaWoo, Jong KyuJung, YuchaeJeong, DawoonKang, MinsookYoo, Young-JiLee, HaniOh, Seung HyunRyu, Jae-HaKim, Woo-Young
Issue Date
Jan-2016
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Evodiamine; Cancer stem-like cells; Rb; Breast cancer
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.469, no.4, pp 1153 - 1158
Pages
6
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
469
Number
4
Start Page
1153
End Page
1158
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9979
DOI
10.1016/j.bbrc.2015.12.066
ISSN
0006-291X
1090-2104
Abstract
In spite of the recent improvements, the resistance to chemotherapy/radiotherapy followed by relapse is the main hurdle for the successful treatment of breast cancer, a leading cause of death in women. A small population of breast cancer cells that have stem-like characteristics (cancer stem-like cells; CSLC) may contribute to this resistance and relapse. Here, we report on a component of a traditional Chinese medicine, evodiamine, which selectively targets CSLC of breast cancer cell lines MCF7 and MDAMB 231 at a concentration that does show a little or no cytotoxic effect on bulk cancer cells. While evodiamine caused the accumulation of bulk cancer cells at the G2/M phase, it did not hold CSLC in a specific cell cycle phase but instead, selectively killed CSLC. This was not due to the culture of CSLC in suspension or without FBS. A proteomic analysis and western blotting revealed that evodiamine changed the expression of cell cycle regulating molecules more efficiently in CSLC cells than in bulk cancer cells. Surprisingly, evodiamine selectively activated p53 and p21 and decreased inactive Rb, the master molecules in G1/S checkpoint. These data collectively suggest a novel mechanism involving CSLC-specific targeting by evodiamine and its possible use to the therapy of breast cancer. (C) 2015 Elsevier Inc. All rights reserved.
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