Evidence map›Paper›PMID 32595209›Full record

ArticleBritish journal of cancer2020

Syntenin-1 promotes colorectal cancer stem cell expansion and chemoresistance by regulating prostaglandin E2 receptor.

Kazuya Iwamoto, Hidekazu Takahashi, Daisuke Okuzaki, Hideo Osawa, Takayuki Ogino, Norikatsu Miyoshi, Mamoru Uemura, Chu Matsuda, Hirofumi Yamamoto, Tsunekazu Mizushima and 3 more

Abstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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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

13 authors.

Kazuya IwamotoDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hidekazu TakahashiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan. htakahashi@gesurg.med.osaka-u.ac.jp.
Daisuke OkuzakiDepartment of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Hideo OsawaDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Takayuki OginoDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Norikatsu MiyoshiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Mamoru UemuraDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Chu MatsudaDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hirofumi YamamotoDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Tsunekazu MizushimaDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Masaki MoriDepartment of Surgery and Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Yuichiro DokiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe protein syntenin-1 is expressed by a variety of cell types, and is upregulated in various malignancies, including melanoma, breast cancer and glioma. Although the mechanism by which elevated syntenin-1 expression contributes to cancer has been described, the exact pathway has not been elucidated.

methodsTo investigate the involvement of syntenin-1 in colorectal cancer (CRC), we performed immunohistochemical analysis of 139 CRC surgical specimens. We also examined syntenin-1 knockdown in CRC cell lines.

resultsHigh syntenin-1 expression was associated with less differentiated histologic grade and poor prognosis, and was an independent prognostic indicator in CRC. Syntenin-1 knockdown in CRC cells reduced the presence of cancer stem cells (CSCs), oxaliplatin chemoresistance and migration. DNA microarray analysis and quantitative real-time polymerase chain reaction showed decreased prostaglandin E2 receptor 2 (PTGER2) expression in syntenin-1-knockdown cells. PTGER2 knockdown in CRC cells yielded the same phenotype as syntenin-1 knockdown. Celecoxib, which has anti-inflammatory effects by targeting cyclooxygenase-2, reduced CSCs and decreased chemoresistance, while prostaglandin E2 (PGE2) had the opposite effect.

conclusionsOur findings suggested that syntenin-1 enhanced CSC expansion, oxaliplatin chemoresistance and migration capability through regulation of PTGER2 expression. Syntenin-1 may be a promising new prognostic factor and target for anti-cancer therapies.

Indexed as

AgedCell Line, TumorCell MovementColorectal NeoplasmsDrug Resistance, NeoplasmFemaleHEK293 CellsHumansMaleMiddle AgedNeoplastic Stem CellsOxaliplatinPrognosisReceptors, Prostaglandin ESynteninsOxaliplatinReceptors, Prostaglandin ESyntenins

Identifiers

PMID32595209
PMCPMC7492211

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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.