Evidence map›Paper›PMID 26135631›Full record

ArticleScientific reports2015

Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mRNA.

Meng Shen, Meng-Yao Wu, Long-Pei Chen, Qiaoming Zhi, Fei-Ran Gong, Kai Chen, Dao-Ming Li, Yadi Wu, Min Tao, Wei Li

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Meng ShenDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Meng-Yao WuDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Long-Pei ChenDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Qiaoming ZhiDepartment of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Fei-Ran GongDepartment of Hematology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Kai ChenDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Dao-Ming LiDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Yadi WuDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Min Tao1] Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China [2] Jiangsu Institute of Clinical Immunology, Suzhou 215006, China [3] Institute of Medical Biotechnology, Soochow University, Suzhou 215021, China [4] PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou 215021, China.
Wei Li1] Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China [2] PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou 215021, China.
First Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cantharidin is an active constituent of mylabris, a traditional Chinese medicine, and is a potent and selective inhibitor of protein phosphatase 2A (PP2A) that plays an important role in cell cycle control, apoptosis, and cell-fate determination. In the present study, we found that cantharidin repressed the invasive ability of pancreatic cancer cells and downregulated matrix metalloproteinase 2 (MMP2) expression through multiple pathways, including ERK, JNK, PKC, NF-κB, and β-catenin. Interestingly, transcriptional activity of the MMP2 promoter increased after treatment with PP2A inhibitors, suggesting the involvement of a posttranscriptional mechanism. By using an mRNA stability assay, we found accelerated degradation of MMP2 mRNA after treatment of cantharidin. Microarray analyses revealed that multiple genes involved in the 3' → 5' decay pathway were upregulated, especially genes participating in cytoplasmic deadenylation. The elevation of these genes were further demonstrated to be executed through ERK, JNK, PKC, NF-κB, and β-catenin pathways. Knockdown of PARN, RHAU, and CNOT7, three critical members involved in cytoplasmic deadenylation, attenuated the downregulation of MMP2. Hence, we present the mechanism of repressed invasion by cantharidin and other PP2A inhibitors through increased degradation of MMP2 mRNA by elevated cytoplasmic deadenylation.

Indexed as

Antineoplastic AgentsCantharidinCell Line, TumorDrug Screening Assays, AntitumorEnzyme RepressionHumansMatrix Metalloproteinase 2Neoplasm InvasivenessPancreatic NeoplasmsProtein Phosphatase 2RNA, MessengerRNA StabilitySignal TransductionAntineoplastic AgentsCantharidinMatrix Metalloproteinase 2MMP2 protein, humanPPP2CA protein, humanProtein Phosphatase 2RNA, Messenger

Identifiers

PMID26135631
PMCPMC4488834
OpenAlexW2270394595

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.