Evidence map›Paper›PMID 40241262›Full record

ArticleCancer science2025

p53 Deficiency in Colon Cancer Cells Promotes Tumor Progression Through the Modulation of Meflin in Fibroblasts.

Eiji Kimura, Yoshito Hayashi, Kentaro Nakagawa, Hirotsugu Saiki, Minoru Kato, Ryotaro Uema, Takanori Inoue, Takeo Yoshihara, Akihiko Sakatani, Hiromu Fukuda and 8 more

Abstract read
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

18 authors.

Eiji KimuraDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID https://orcid.org/0000-0002-9832-5422
Yoshito HayashiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Kentaro NakagawaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Hirotsugu SaikiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID https://orcid.org/0009-0001-5517-1646
Minoru KatoDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Ryotaro UemaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Takanori InoueDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Takeo YoshiharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Akihiko SakataniDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Hiromu FukudaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Ayaka TajiriDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Yujiro AdachiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Kazuhiro MuraiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Shunsuke YoshiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID https://orcid.org/0000-0002-7817-1809
Yoshiki TsujiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Shinichiro ShinzakiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Hideki IijimaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.

Funding

Japan Society for the Promotion of Science JP21K15922
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment, play an important role in tumor progression. Colon cancer cells deficient in p53 activate fibroblasts and enhance fibroblast-mediated tumor growth. Meflin is a CAF marker capable of inhibiting tumor growth. In this study, we investigated the role of Meflin in fibroblasts using human cell lines (colon cancer HCT116 and fibroblasts CCD-18Co) and clinical specimens. TP53-suppressed HCT116 (HCT116

Indexed as

Cancer-Associated FibroblastsColonic NeoplasmsTumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationCoculture TechniquesDisease ProgressionFemaleFibroblastsGene Expression Regulation, NeoplasticHCT116 CellsHumansMaleMiceMice, NudeTP53 protein, humanTumor Suppressor Protein p53colon cancerfibroblastsMeflinp53tumor microenvironment

Identifiers

PMID40241262
PMCPMC12210049

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.