Evidence map›Paper›PMID 21304177›Full record

ArticleOncotarget2010

A novel screen using the Reck tumor suppressor gene promoter detects both conventional and metastasis-suppressing anticancer drugs.

Ryuya Murai, Yoko Yoshida, Teruyuki Muraguchi, Emi Nishimoto, Yoko Morioka, Hitoshi Kitayama, Shinae Kondoh, Yoshinori Kawazoe, Masahiro Hiraoka, Motonari Uesugi and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
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  10. miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2015
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Ryuya MuraiDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Yoko YoshidaDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Teruyuki MuraguchiDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Emi NishimotoDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Yoko MoriokaDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Hitoshi KitayamaDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Shinae KondohDepartment of Radiation Oncology and Image-Applied Therapy, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Yoshinori KawazoeInstitutes for Chemical Research, Institute for Integrated Cell-Material Sciences, and Global COE Program, Kyoto University, Uji, Kyoto 611-0011, Japan.
Masahiro HiraokaDepartment of Radiation Oncology and Image-Applied Therapy, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Motonari UesugiInstitutes for Chemical Research, Institute for Integrated Cell-Material Sciences, and Global COE Program, Kyoto University, Uji, Kyoto 611-0011, Japan.
Makoto NodaDepartment of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The membrane-anchored matrix metalloproteinase-regulator RECK is often downregulated in various types of cancers; the levels of residual RECK in resected tumors often correlate with better prognosis. Forced expression of RECK in cancer cells suppresses tumor angiogenesis, invasion, and metastasis in xenograft models. RECK is therefore a promising marker for benignancy and a potential effector in cancer therapy. We established a cell line containing two transgene systems: (1) the secreted alkaline phosphatase (SEAP) gene fused to Reck promoter and (2) the HRAS(12V) oncogene driven by the Tet-off promoter system. This cell line exhibits transformed phenotype in regular medium and flat morphology with increased SEAP activity in the presence of doxycycline, allowing the assessment of RECK-inducing activity of chemicals in the contexts of both transformed and untransformed cells. Our pilot experiments with 880 known bioactive compounds detected 34 compounds that activate RECK promoter; among these, 10 were authentic anticancer drugs. Four selected compounds up-regulated endogenous RECK protein in several human cancer cell lines. The top-ranking compound, disulfiram, strongly suppressed spontaneous lung-metastasis of human fibrosarcoma cells in nude mice. Our data demonstrate the value of this screen in discovering effective cancer therapeutics.

Indexed as

Promoter Regions, GeneticAlkaline PhosphataseAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationDisulfiramDoxycyclineDrug DiscoveryDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansImmunoblottingMiceNeoplasm MetastasisAlkaline PhosphataseAntineoplastic AgentsDisulfiramDoxycyclineGPI-Linked ProteinsHRAS protein, humanProto-Oncogene Proteins p21(ras)RECK protein, human

Identifiers

PMID21304177
PMCPMC3248105

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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.