Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/101974
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Type: Journal article
Title: Identification of candidate anti-cancer molecular mechanisms of compound kushen injection using functional genomics
Author: Qu, Z.
Cui, J.
Harata-Lee, Y.
Thazin Nwe Aung, T.
Feng, Q.
Raison, J.
Kortschak, R.
Adelson, D.
Citation: Oncotarget, 2016; 7(40):66003-66019
Publisher: Impact Journals
Issue Date: 2016
ISSN: 1949-2553
1949-2553
Statement of
Responsibility: 
Zhipeng Qu, Jian Cui, Yuka Harata-Lee, Thazin Nwe Aung, Qianjin Feng, Joy M. Raison, Robert Daniel Kortschak, David L. Adelson
Abstract: Compound Kushen Injection (CKI) has been clinically used in China for over 15 years to treat various types of solid tumours. However, because such Traditional Chinese Medicine (TCM) preparations are complex mixtures of plant secondary metabolites, it is essential to explore their underlying molecular mechanisms in a systematic fashion. We have used the MCF-7 human breast cancer cell line as an initial in vitro model to identify CKI induced changes in gene expression. Cells were treated with CKI for 24 and 48 hours at two concentrations (1 and 2 mg/mL total alkaloids), and the effect of CKI on cell proliferation and apoptosis were measured using XTT and Annexin V/Propidium Iodide staining assays respectively. Transcriptome data of cells treated with CKI or 5-Fluorouracil (5-FU) for 24 and 48 hours were subsequently acquired using high-throughput Illumina RNA-seq technology. In this report we show that CKI inhibited MCF-7 cell proliferation and induced apoptosis in a dose-dependent fashion. We integrated and applied a series of transcriptome analysis methods, including gene differential expression analysis, pathway over-representation analysis, de novo identification of long non-coding RNAs (lncRNA) as well as co-expression network reconstruction, to identify candidate anti-cancer molecular mechanisms of CKI. Multiple pathways were perturbed and the cell cycle was identified as the potential primary target pathway of CKI in MCF-7 cells. CKI may also induce apoptosis in MCF-7 cells via a p53 independent mechanism. In addition, we identified novel lncRNAs and showed that many of them might be expressed as a response to CKI treatment.
Keywords: systems biology; traditional chinese medicine; lncRNA; transcriptome
Rights: licensed under a Creative Commons Attribution 3.0 License.
DOI: 10.18632/oncotarget.11788
Appears in Collections:Aurora harvest 7
Earth and Environmental Sciences publications

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