Evidence map›Paper›PMID 25350954›Full record

ArticleOncotarget2014

Thymidine phosphorylase activates NFκB and stimulates the expression of angiogenic and metastatic factors in human cancer cells.

Sho Tabata, Ryuji Ikeda, Masatatsu Yamamoto, Shunji Shimaoka, Naofumi Mukaida, Yasuo Takeda, Katsushi Yamada, Tomoyoshi Soga, Tatsuhiko Furukawa, Shin-ichi Akiyama

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 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

10 authors at 5 institutions in 1 country.

Sho TabataInstitute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata 997-0052, Japan.
Ryuji IkedaDepartment of Clinical Pharmacy and Pharmacology, Graduate School Medical and Dental Science, Kagoshima University, Kagoshima 890-8544, Japan.
Masatatsu YamamotoDepartment of Molecular Oncology, Graduate School Medical and Dental Science, Kagoshima University, Kagoshima 890-8544, Japan.
Shunji ShimaokaDepartment of Gastroenterology, Nanpuh Hospital, Kagoshima 892-0854, Japan.
Naofumi MukaidaDepartment of Molecular Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Yasuo TakedaDepartment of Clinical Pharmacy and Pharmacology, Graduate School Medical and Dental Science, Kagoshima University, Kagoshima 890-8544, Japan.
Katsushi YamadaDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Nagasaki International University, Sasebo, Nagasaki 859-3298, Japan.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata 997-0052, Japan.
Tatsuhiko FurukawaDepartment of Molecular Oncology, Graduate School Medical and Dental Science, Kagoshima University, Kagoshima 890-8544, Japan.
Shin-ichi AkiyamaClinical Research Center, National Kyushu Cancer Center, Notame Minami-ku, Fukuoka 811-1395, Japan.
Kagoshima University · JPKeio University · JPKanazawa University · JPNagasaki International University · JPNational Hospital Organization Kyushu Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymidine phosphorylase (TP) promotes angiogenesis and metastasis, and confers resistance to anticancer agents in some cancer cell types. We previously reported that TP stimulates the expression of interleukin (IL)-8 in human KB cancer cells by an unknown mechanism. A mutation in the nuclear factor (NF)κB binding site of the IL-8 promoter suppressed promoter activity in KB/TP cells that overexpress TP. Specifically inhibiting NFκB by using BY11-7082 also suppressed TP-induced IL-8 promoter activity and IL-8 expression. Moreover, TP overexpression led to the activation of NFκB and an upregulation in the expression of its target genes, and increased phosphorylated IKKα/β protein levels, while promoting IκBα degradation as well as p65 phosphorylation and nuclear localization. The activation of NFκB in KB/TP cells was suppressed by the antioxidants N-acetylcysteine and EUK-8. In addition, in gastric cancer tissue samples, the expression of the NFκB-regulated genes, including IL-8, IL-6, and fibronectin-1 was positively correlated with TP expression. These findings indicate that reactive oxygen species mediated NFκB activation by TP increases the expression of genes that promote angiogenesis and metastasis in gastric cancer.

Indexed as

ApoptosisBlotting, WesternCell ProliferationFibronectinsGene Expression Regulation, NeoplasticHumansInterleukin-6Interleukin-8Neovascularization, PathologicNF-kappa BPhosphorylationPromoter Regions, GeneticReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionFibronectinsInterleukin-6Interleukin-8NF-kappa BRNA, MessengerThymidine Phosphorylase

Identifiers

PMID25350954
PMCPMC4279387
OpenAlexW2141587124

What OpenQuestion holds

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LicenceCC BY
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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.