Evidence map›Paper›PMID 34689171›Full record

ArticleBritish journal of cancer2021

Mitochondrial matrix protein C14orf159 attenuates colorectal cancer metastasis by suppressing Wnt/β-catenin signalling.

Kenji Ohshima, Ryo Oi, Daisuke Okuzaki, Daisuke Motooka, Masakazu Shinohara, Satoshi Nojima, Eiichi Morii

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2021. 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
0.1field-weighted citation impact, top 55% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  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

7 authors at 2 institutions in 1 country.

Kenji OhshimaDepartment of Pathology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. ohshima-k@molpath.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-1114-386X
Ryo OiDepartment of Pathology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-4552-783X
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Masakazu ShinoharaDivision of Epidemiology, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan.
Satoshi NojimaDepartment of Pathology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. morii@molpath.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-8490-3650
The University of Osaka · JPKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mechanisms underlying metastasis of colorectal cancer (CRC) remain unclear. C14orf159 is a mitochondrial matrix protein converting D-glutamate to 5-oxo-D-proline. Other metabolic functions of C14orf159, especially on mitochondrial metabolism, and its contribution to CRC metastasis, are not elucidated.

methodsMetabolome analysis by gas chromatography-mass spectrometry, RNA-sequencing analysis, flow cytometry, migration and invasion assay, sphere-formation assay using C14orf159-knockout and -stable expressing cells, immunohistochemistry of C14orf159 in human CRC specimens, and xenograft experiments using Balb/c nude mice were conducted.

resultsC14orf159 maintained the mitochondrial membrane potential of human CRC cells, and its involvement in amino acid and glutathione metabolism was demonstrated. In human CRC specimens, a decrease in C14orf159 expression at the invasive front of the tumour and in metastasis was determined. C14orf159 was also shown to attenuate the migration, invasion, and spheroid growth of CRC cells in vitro and colorectal tumour growth and metastasis in vivo. Mechanistically, C14orf159 reduced the expression of genes involved in CRC metastasis, including members of the Wnt and MMP family, by maintaining the mitochondrial membrane potential.

conclusionsOur findings link mitochondrial membrane potential to Wnt/β-catenin signalling and reveal a previously unrecognised function of the mitochondrial matrix protein C14orf159 as a suppressor of CRC metastasis.

Indexed as

Animalsbeta CateninCell Line, TumorColorectal NeoplasmsDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHumansMiceMitochondrial ProteinsNeoplasm MetastasisWnt Signaling PathwayXenograft Model Antitumor Assaysbeta CateninMitochondrial Proteins

Identifiers

PMID34689171
PMCPMC8651639
OpenAlexW3209416786

What OpenQuestion holds

Textmetadata
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.