alexa Beta-Hydroxyisovalerylshikonin Inhibits the Growth of U266 Multiple Myeloma Cells by Triggering the Mitochondrial Pathway
ISSN: 2329-6917

Journal of Leukemia
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Research Article

Beta-Hydroxyisovalerylshikonin Inhibits the Growth of U266 Multiple Myeloma Cells by Triggering the Mitochondrial Pathway

Yihui He1*, Xiaoyan Chen1 and Lingying Kong2

1Department of Pathology, Fujian Provincial Hospital, Fuzhou, Fujian 350001, China

2Department of Pathology, Affiliated People’s Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350004, P.R. China

Corresponding Author:
Yihui He
Department of Pathology, Fujian Provincial Hospital
No.134, Dongjie, Gulou, Fuzhou, Fujian 350001, P.R. China
Tel: 8615960061055
E-mail: [email protected]

Received Date: July 10, 2014; Accepted Date: September 05, 2014; Published Date: September 10, 2014

Citation: He Y, Chen X, Kong L (2014) Beta-Hydroxyisovalerylshikonin Inhibits the Growth of U266 Multiple Myeloma Cells by Triggering the Mitochondrial Pathway. J Leuk (Los Angel) 2:155. doi: 10.4172/2329-6917.1000155

Copyright: © 2014 He Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Background: Beta-hydroxyisovalerylshikonin (beta-HIVS) is a compound isolated from the traditional oriental medicinal herb lithospermum radix. This drug exerts a role as an ATP non-competitive inhibitor of Protein-Tyrosine Kinases (PTKs) and shows great potential for induction of apoptosis against human cancer cells. We investigated the effect of beta-HIVS on multiple myeloma U266 cells and clarified details of the primary mechanism in its apoptosisinducing activity. Objective: The aim of this work was to trace the apoptosis-inducing activity of beta-HIVS on U266 cells as well as the underlying mechanisms. Methods: Cell Counting Kit-8 (CCK-8) test and colony-forming assay were performed in estimating the effects of beta-HIVS on U266 cell viability and colony formation. Apoptosis analysis was carried out on the basis of DAPI fluorescence staining and DNA fragmentation assays. Real-time PCR was employed to evaluate changes of Bcl-2 and Bax mRNA expression, while indirect immunofluorescence assay and western blotting were utilized in validating the expression of Bcl-2, Bax, caspase-3, caspase-9, PARP and cytochrome c. Results: CCK-8 test and colony-forming assay showed that beta-HIVS treatment resulted in significantly reduced cell proliferation (P<0.05 or 0.01) and colony formation (P<0.01). Real-time PCR results indicated that the expression level of Bcl-2 mRNA was reduced at 72h following beta-HIVS co-cultivation (P<0.01), although Bax mRNA altered with no significance. Immunofluorescence assay displayed that caspase-3 was activated in beta- HIVS treated group, accompanied by an increased expression of cytochrome c. Western blotting also exhibited that the expression of Bcl-2 protein in beta-HIVS treated group decreased and cytochrome c increased at 72h after co-cultivation. Moreover, caspase-3 and -9, as well as PARP were activated, all with P<0.01 when compared with the two control groups. Conclusion: Beta-HIVS revealed remarkable apoptosis-inducing activity in U266 cells, possibly by inhibiting proliferation and promoting apoptosis via the mitochondrial pathway.


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