TY - JOUR
T1 - Anticancer effect of (E)-2-hydroxy-3′,4,5′-trimethoxystilbene on breast cancer cells by mitochondrial depolarization
AU - Chae, Yee Soo
AU - Kim, Jong Gwang
AU - Jung, Hyun Jun
AU - Yang, Jung Dug
AU - Jung, Jin Hyang
AU - Aiyar, Sarah E.
AU - Kim, Sanghee
AU - Park, Hoyong
PY - 2011/8
Y1 - 2011/8
N2 - Background: TMS (2,3′,4,5′-tetramethoxystilbene), a stilbene analog derived from rhapontigenin, was previously demonstrated to induce apoptosis in hormone-resistant breast cancer cells. Therefore, this study investigated the anticancer effect of a new stilbene analog, HTMS ((E)-2-hydroxy-3′,4,5′-trimethoxystilbene), and its mechanism in various breast cancer cell lines. Materials and methods: The effect of HTMS on cell proliferation of MDA-MB-231, MCF-7, and LTED cells was evaluated using MTT assays. Cell apoptosis was detected by FITC-annexin V staining and flow cytometry analysis, changes in mitochondrial potential were determined by fluorescence microscopy using TMRE staining, and the expression of cleaved PARP and release of cytochrome c were assessed by Western blot analysis. Results: HTMS significantly decreased the cell viability of various types of breast cancer cells in a dose- and time-dependent manner, characterized by G2/M arrest of the cell cycle and the induction of apoptosis. In particular, HTMS disturbed the mitochondrial membrane potential, causing a release of cytochrome c during apoptosis. Furthermore, HTMS was superior to TMS in inhibiting cancer cell growth in a pilot comparison study. Conclusion: HTMS is an effective apoptotic agent for breast cancer cells, making it a candidate therapeutic agent for the treatment of breast cancer.
AB - Background: TMS (2,3′,4,5′-tetramethoxystilbene), a stilbene analog derived from rhapontigenin, was previously demonstrated to induce apoptosis in hormone-resistant breast cancer cells. Therefore, this study investigated the anticancer effect of a new stilbene analog, HTMS ((E)-2-hydroxy-3′,4,5′-trimethoxystilbene), and its mechanism in various breast cancer cell lines. Materials and methods: The effect of HTMS on cell proliferation of MDA-MB-231, MCF-7, and LTED cells was evaluated using MTT assays. Cell apoptosis was detected by FITC-annexin V staining and flow cytometry analysis, changes in mitochondrial potential were determined by fluorescence microscopy using TMRE staining, and the expression of cleaved PARP and release of cytochrome c were assessed by Western blot analysis. Results: HTMS significantly decreased the cell viability of various types of breast cancer cells in a dose- and time-dependent manner, characterized by G2/M arrest of the cell cycle and the induction of apoptosis. In particular, HTMS disturbed the mitochondrial membrane potential, causing a release of cytochrome c during apoptosis. Furthermore, HTMS was superior to TMS in inhibiting cancer cell growth in a pilot comparison study. Conclusion: HTMS is an effective apoptotic agent for breast cancer cells, making it a candidate therapeutic agent for the treatment of breast cancer.
KW - Apoptosis
KW - Breast cancer
KW - HTMS
KW - Stilbene analog
UR - http://www.scopus.com/inward/record.url?scp=79960909807&partnerID=8YFLogxK
U2 - 10.1007/s00280-010-1464-0
DO - 10.1007/s00280-010-1464-0
M3 - Article
C2 - 20978764
AN - SCOPUS:79960909807
SN - 0344-5704
VL - 68
SP - 349
EP - 358
JO - Cancer Chemotherapy and Pharmacology
JF - Cancer Chemotherapy and Pharmacology
IS - 2
ER -