Evidence map›Paper›PMID 23686315›Full record

ArticleOncogene2014

ANGPTL4 is a secreted tumor suppressor that inhibits angiogenesis.

E Okochi-Takada, N Hattori, T Tsukamoto, K Miyamoto, T Ando, S Ito, Y Yamamura, M Wakabayashi, Y Nobeyama, T Ushijima

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.0field-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

63 citing papers in PubMed, 91 citations in OpenAlex.

  1. Targeting the ANGPTL4/NRP1/ABL1/RAD51 axis reverses cisplatin resistance by impairing DNA damage repair in head and neck cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Research (Washington, D.C.) · 2024
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3 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

E Okochi-TakadaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
N HattoriDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
T TsukamotoOncological Pathology Division, Aichi Cancer Center Research Institute, Nagoya, Japan.
K MiyamotoDivision of Molecular Oncology, National Hospital Organization Kure Medical Center and Chugoku Cancer Center, Kureshi, Japan.
T Ando1] Division of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan [2] Third Department of Internal Medicine, University of Toyama, Toyama, Japan.
S ItoDepartment of Gastroenterological Surgery, Aichi Cancer Center Central Hospital, Nagoya, Japan.
Y YamamuraDepartment of Gastroenterological Surgery, Aichi Cancer Center Central Hospital, Nagoya, Japan.
M WakabayashiDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Y Nobeyama1] Division of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan [2] Department of Dermatology, The Jikei University School of Medicine, Tokyo, Japan.
T UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Aichi Cancer Center · JPJikei University School of Medicine · JPNational Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor suppressors with extracellular function are likely to have advantages as targets for cancer therapy, but few are known. Here, we focused on angiopoietin-like 4 (ANGPTL4), which is a secreted glycoprotein involved in lipoprotein metabolism and angiogenesis, is methylation-silenced in human cancers, but has unclear roles in cancer development and progression. We found a deletion mutation in its coiled-coil domain at its N-terminal in human gastric cancers, in addition to hypermethylation of the ANGPTL4 promoter CpG islands. Forced expression of wild-type ANGPTL4, but not ANGPTL4 with the deletion, at physiological levels markedly suppressed in vivo tumorigenicity and tumor angiogenesis, indicating that the latter caused the former. Tumor-derived ANGPTL4 suppressed in vitro vascular tube formation and proliferation of human umbilical vascular endothelial cells, partly due to suppression of ERK signaling. These showed that ANGPTL4 is a genetically and epigenetically inactivated secreted tumor suppressor that inhibits tumor angiogenesis.

Indexed as

AgedAmino Acid SequenceAngiopoietin-Like Protein 4AngiopoietinsAnimalsBase SequenceCase-Control StudiesCpG IslandsDNA MethylationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CAngiopoietin-Like Protein 4AngiopoietinsANGPTL4 protein, humanTumor Suppressor Proteins

Identifiers

PMID23686315
OpenAlexW2049460097

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.