Evidence map›Paper›PMID 37921070›Full record

ArticleInternational journal of oncology2023

The apelin‑apelin receptor signaling pathway in fibroblasts is involved in tumor growth via p53 expression of cancer cells.

Hirotsugu Saiki, Yoshito Hayashi, Shunsuke Yoshii, Eiji Kimura, Kentaro Nakagawa, Minoru Kato, Ryotaro Uema, Takanori Inoue, Akihiko Sakatani, Takeo Yoshihara and 4 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 11 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

14 authors at 2 institutions in 1 country.

Hirotsugu Saiki *Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Yoshito HayashiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Shunsuke Yoshii *Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Eiji KimuraDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Kentaro NakagawaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Minoru KatoDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Ryotaro UemaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Takanori InoueDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Akihiko SakataniDepartment of Gastroenterology and Hepatology, Osaka Police Hospital, Tennoji, Osaka 543‑0035, Japan.
Takeo YoshiharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Yoshiki TsujiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Shinichiro ShinzakiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Hideki IijimaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka 565‑0871, Japan.
Osaka University · JPOsaka Police Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer‑associated fibroblasts (CAFs) are pivotal in tumor progression. TP53‑deficiency in cancer cells is associated with robust stromal activation. The apelin‑apelin receptor (APJ) system has been implicated in suppressing fibroblast‑to‑myofibroblast transition in non‑neoplastic organ fibrosis. The present study aimed to elucidate the oncogenic role of the apelin‑APJ system in tumor fibroblasts. APJ expression and the effect of APJ suppression in fibroblasts were investigated for p53 status in cancer cells using human cell lines (TP53‑wild colon cancer, HCT116, and Caco‑2; TP53‑mutant colon cancer, SW480, and DLD‑1; and colon fibroblasts, CCD‑18Co), resected human tissue samples of colorectal cancers, and immune‑deficient nude mouse xenograft models. The role of exosomes collected by ultracentrifugation were also analyzed as mediators of p53 expression in cancer cells and APJ expression in fibroblasts. APJ expression in fibroblasts co‑cultured with p53‑suppressed colon cancer cells (HCT116

Indexed as

Cancer-Associated FibroblastsColonic NeoplasmsMicroRNAsAnimalsApelinApelin ReceptorsCaco-2 CellsCell ProliferationFibroblastsHumansMiceSignal TransductionTumor MicroenvironmentTumor Suppressor Protein p53ApelinApelin ReceptorsMicroRNAsTumor Suppressor Protein p53cancer‑associated fibroblastscolonic neoplasmsexosomesmicroRNAstumor microenvironment

Identifiers

PMID37921070
PMCPMC10631769
OpenAlexW4388225670

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.