Evidence map›Paper›PMID 28790850›Full record

ArticleOncoTargets and therapy2017

Emodin suppresses proliferation, migration and invasion in ovarian cancer cells by down regulating ILK in vitro and in vivo.

Jingjing Lu, Ying Xu, Zhe Zhao, Xiaoning Ke, Xuan Wei, Jia Kang, Xuan Zong, Hongluan Mao, Peishu Liu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in OncoTargets and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  19. Emodin Impairs Radioresistance of Human Osteosarcoma Cells by Suppressing Sonic Hedgehog Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Jingjing LuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Ying XuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Zhe ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Xiaoning KeDepartment of Obstetrics and Gynecology, Handan Central Hospital, Handan, People's Republic of China.
Xuan WeiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Jia KangDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Xuan ZongDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Hongluan MaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Peishu LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong.
Qilu Hospital of Shandong University · CNHandan College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAlthough our previous studies have confirmed that 1, 3, 8-trihydroxy-6-methylant hraquinone (emodin) inhibits migration and invasion in epithelial ovarian cancer (EOC) cells, the underlying molecular mechanism remains unknown. Here, the aim was to investigate the effects of emodin on EOC cells and to study further the mechanism underlying this process, both in vitro and in vivo. MATERIALS AND

methodsCell proliferation was evaluated by the methylthiazolyl tetrazolium assay. Cell migration and invasion abilities were tested using the transwell assay. The expression of integrin-linked kinase (ILK) and epithelial-mesenchymal transition (EMT)-associated factors were measured with western blotting.

resultsExogenous ILK enhanced the proliferation, migration and invasion properties of A2780 and SK-OV-3 cells. After treatment with emodin, the survival rate of cells was gradually reduced, including those of SK-OV-3/pLVX-ILK and A2780/pLVX-ILK cells, with increasing emodin concentrations. The migration and invasion abilities of A2780 and SK-OV-3 cells were effectively increased by the transfection of pLVX-ILK, which could be abrogated by following this with 48 hours of emodin treatment. Treatment with emodin significantly downregulated the expression of ILK and EMT-related proteins. So, emodin suppressed proliferation, migration and invasion in ovarian cancer cells by downregulating ILK in vitro. SK-OV-3/pLVX-Con and SK-OV-3/pLVX-ILK cells were used to generate xenografts in nude mice. Tumors grew more rapidly in the SK-OV-3/pLVX-ILK group compared with the control group, and this could be significantly inhibited by emodin. Also, the expression of E-cadherin was downregulated, while the expression of Slug, MMP-9 and Vimentin were upregulated in the SK-OV-3/pLVX-ILK group, and this could be reversed by following treatment with emodin. Emodin did not demonstrate target toxicity on hepatocytes, nephrocytes and cardiomyocytes.

conclusionEmodin suppresses proliferation, migration and invasion in ovarian cancer by targeting ILK.

Indexed as

emodinepithelial–mesenchymal transitionepithelial ovarian cancerILKSlugxenografts in nude mice

Identifiers

PMID28790850
PMCPMC5530856
OpenAlexW2738682729

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.