Evidence map›Paper›PMID 27602759›Full record

ArticleOncotarget2016

Identification of candidate anti-cancer molecular mechanisms of Compound Kushen Injection using functional genomics.

Zhipeng Qu, Jian Cui, Yuka Harata-Lee, Thazin Nwe Aung, Qianjin Feng, Joy M Raison, Robert Daniel Kortschak, David L Adelson

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 3 pooled it
8.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Zhipeng QuDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Jian CuiDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Yuka Harata-LeeDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Thazin Nwe AungDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Qianjin FengShanxi Modern Chinese Medicine Engineering Laboratory, Shanxi University of Traditional Chinese Medicine, Shanxi 030619, China.
Joy M RaisonDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Robert Daniel KortschakDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
David L AdelsonDepartment of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
University of Adelaide · AUShanxi University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Gene Expression ProfilingAntineoplastic AgentsApoptosisBiomarkers, TumorBreast NeoplasmsCell CycleCell ProliferationChinaDrugs, Chinese HerbalFemaleGenomicsHumansRNA, Long NoncodingTumor Cells, CulturedAntineoplastic AgentsBiomarkers, TumorDrugs, Chinese HerbalkushenRNA, Long NoncodinglncRNAsystems biologytranscriptome

Identifiers

PMID27602759
PMCPMC5323210
OpenAlexW2518211915

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.