Evidence map›Paper›PMID 28507327›Full record

ArticleScientific reports2017

PDE3 inhibitor and EGCG combination treatment suppress cancer stem cell properties in pancreatic ductal adenocarcinoma.

Motofumi Kumazoe, Mika Takai, Shun Hiroi, Chieri Takeuchi, Maasa Yamanouchi, Takashi Nojiri, Hiroaki Onda, Jaehoon Bae, Yuhui Huang, Kanako Takamatsu and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Pan-cancer ex vivo target evaluation of phosphodiesterase 3 A (PDE3A).Journal of molecular medicine (Berlin, Germany) · 2026
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  9. Src Mediates Epigallocatechin-3-Molecules (Basel, Switzerland) · 2020
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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

16 authors at 4 institutions in 1 country.

Motofumi KumazoeDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Mika TakaiDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Shun HiroiDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Chieri TakeuchiDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Maasa YamanouchiDepartment of Applied Chemistry, Graduate School of Science and Engineering, Tokyo Institute of Technology, 2-12-1 Ookayama, Meguro, Tokyo, 152-8552, Japan.
Takashi NojiriDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita-City, Osaka, 565-8565, Japan.
Hiroaki OndaDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita-City, Osaka, 565-8565, Japan.
Jaehoon BaeDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Yuhui HuangDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Kanako TakamatsuDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Shuya YamashitaDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Shuhei YamadaDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.
Kenji KangawaDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita-City, Osaka, 565-8565, Japan.
Takashi TakahashiYokohama College of Pharmacy 601, Matana-cho, Totsuka-ku, Yokohama, Kanagawa, 245-0066, Japan.
Hiroshi TanakaDepartment of Applied Chemistry, Graduate School of Science and Engineering, Tokyo Institute of Technology, 2-12-1 Ookayama, Meguro, Tokyo, 152-8552, Japan.
Hirofumi TachibanaDivision of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan. tatibana@agr.kyushu-u.ac.jp.
Kyushu University · JPNational Cerebral and Cardiovascular Center · JPTokyo Institute of Technology · JPYokohama University of Pharmacy · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recurrence following chemotherapy is observed in the majority of patients with pancreatic ductal adenocarcinoma (PDAC). Recent studies suggest that cancer stem cells (CSCs) may be involved in PDAC recurrence and metastasis. However, an efficient approach to targeting pancreatic CSCs remains to be established. Here we show that in cancer cells overexpressing the 67-kDa laminin receptor (67LR)-dependent cyclic GMP (cGMP) inducer, epigallocatechin-3-O-gallate (EGCG) and a phosphodiesterase 3 (PDE3) inhibitor in combination significantly suppressed the Forkhead box O3 and CD44 axis, which is indispensable for the CSC properties of PDAC. We confirmed that the EGCG and PDE3 inhibitor in combination strongly suppressed tumour formation and liver metastasis in vivo. We also found that a synthesized EGCG analog capable of inducing strong cGMP production drastically suppressed the CSC properties of PDAC and extended the survival period in vivo. In conclusion, the combination treatment of EGCG and a PDE3 inhibitor as a strong cGMP inducer could be a potential treatment candidate for the eradication of CSCs of PDAC.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, Pancreatic DuctalCatechinCell Line, TumorCyclic GMPCyclic Nucleotide Phosphodiesterases, Type 3Disease Models, AnimalDrug SynergismFluorescent Antibody TechniqueGene ExpressionHumansMiceNeoplastic Stem CellsPhosphodiesterase 3 InhibitorsXenograft Model Antitumor AssaysBiomarkers, TumorCatechinCyclic GMPCyclic Nucleotide Phosphodiesterases, Type 3epigallocatechin gallatePhosphodiesterase 3 Inhibitors

Identifiers

PMID28507327
PMCPMC5432527
OpenAlexW2613367258

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.