Evidence map›Paper›PMID 31148360›Full record

ArticleCancer science2019

Exosomal microRNAs derived from colon cancer cells promote tumor progression by suppressing fibroblast TP53 expression.

Shunsuke Yoshii, Yoshito Hayashi, Hideki Iijima, Takanori Inoue, Keiichi Kimura, Akihiko Sakatani, Kengo Nagai, Tetsuji Fujinaga, Satoshi Hiyama, Takahiro Kodama and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 71 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 1 institution in 1 country.

Shunsuke YoshiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID https://orcid.org/0000-0002-7817-1809
Yoshito HayashiDepartment 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.
Takanori InoueDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Keiichi KimuraDepartment 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.
Kengo NagaiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Tetsuji FujinagaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Satoshi HiyamaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Takahiro KodamaDepartment 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.
Yoshiki TsujiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Japan.
Kenji WatabeDepartment 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.
The University of Osaka · JP

Funding

Japan Society for the Promotion of Science JP15K19326Japan Society for the Promotion of Science JP17K15944
6 · The paper itself

Abstract

The tumor microenvironment offers favorable conditions for tumor progression, and activated fibroblasts, known as cancer-associated fibroblasts, play a pivotal role. TP53-deficient cancer cells are known to induce strong fibroblast activation. We aimed to elucidate the oncogenic role of exosomes derived from TP53-deficient colon cancer cells in fibroblast proliferation and tumor growth. Cancer cell-derived exosomes (CDEs) were isolated from the conditioned media of cancer cells using a sequential ultracentrifugation method. The effects of exosomes on tumor growth were evaluated using human cell lines (TP53-WT colon cancer, HCT116; TP53-mutant colon cancer, HT29; and fibroblasts, CCD-18Co and WI-38) and an immune-deficient nude mouse xenograft model. HCT116 (HCT116

Indexed as

AnimalsCancer-Associated FibroblastsCell LineCell Line, TumorCell ProliferationColonic NeoplasmsDisease ProgressionExosomesGene Expression Regulation, NeoplasticHCT116 CellsHeterograftsHT29 CellsHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsTP53 protein, humanTumor Suppressor Protein p53colon cancerexosomal miRNATP53tumor microenvironmenttumor progression

Identifiers

PMID31148360
PMCPMC6676271
OpenAlexW2947024711

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.