Tanshinone IIA, an isolated compound from Salvia miltiorrhiza Bunge, induces apoptosis in HeLa cells through mitotic arrest

Tanshinone IIA (Tan IIA) is a compound isolated from Salvia miltiorrhiza Bunge (Danshen). The aim of this study is to investigate the mechanisms of its anti-cancer effect. To clearly delineate the cell cycle-dependent effects of Tan IIA, we used either synchronized cells or single living cell analys...

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Bibliographic Details
Published in:Life sciences (1973) 2008-09, Vol.83 (11), p.394-403
Main Authors: Zhou, Lingli, Chan, W.K., Xu, Naihan, Xiao, Kang, Luo, Houwei, Luo, Kathy Qian, Chang, Donald C.
Format: Article
Language:English
Subjects:
Anti-cancer drug
Apoptosis
Apoptosis - drug effects
Bcl-2
Blotting, Western
Diterpenes, Abietane
DNA - biosynthesis
Dose-Response Relationship, Drug
Flow Cytometry
Fluorescent Antibody Technique
Green Fluorescent Proteins - metabolism
HeLa Cells
Humans
Interphase - drug effects
Microtubule-interfering agents
Microtubules - drug effects
Mitochondria, Muscle - drug effects
Mitosis - drug effects
Mitotic arrest
Myeloid Cell Leukemia Sequence 1 Protein
Phenanthrenes - isolation & purification
Phenanthrenes - pharmacology
Plasmids - genetics
Proto-Oncogene Proteins c-bcl-2 - metabolism
Salvia miltiorrhiza - chemistry
Subcellular Fractions - drug effects
Subcellular Fractions - metabolism
Tanshinone IIA
Transfection
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Summary:Tanshinone IIA (Tan IIA) is a compound isolated from Salvia miltiorrhiza Bunge (Danshen). The aim of this study is to investigate the mechanisms of its anti-cancer effect. To clearly delineate the cell cycle-dependent effects of Tan IIA, we used either synchronized cells or single living cell analysis to conduct our studies. Subcellular fractionation, Western blot analysis, immuno-fluorescence staining and FACS analysis were also employed in our study. We found that Tan IIA could arrest cancer cells in mitosis by disrupting the mitotic spindle and subsequently triggered cells to enter apoptosis through the mitochondria-dependent apoptotic pathway. Thus, Tan IIA could selectively kill mitotic cells over interphase cells. In comparison with other existing anti-cancer drugs that cause mitotic arrest by interfering with the microtubule structure (such as vincristine or taxol), Tan IIA destroyed only the mitotic spindle during the M phase but not the microtubule structure in interphase cells. Furthermore, Tan IIA could trigger the mitotic arrested cells to enter apoptosis faster than vincristine or taxol. Since Tan IIA can selectively induce cancer cells to enter apoptosis through mitotic arrest, it has the potential to be developed into an anti-cancer drug.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2008.07.011