Evidence map›Paper›PMID 35489200›Full record

ArticleBiochemical and biophysical research communications2022

Inactivation of axon guidance molecule netrin-1 in human colorectal cancer by an epigenetic mechanism.

Hironao Nakayama, Hidetaka Ohnuki, Masako Nakahara, Hisayo Nishida-Fukuda, Tomohisa Sakaue, Shinji Fukuda, Shigeki Higashiyama, Yuki Doi, Masahiro Mitsuyoshi, Takashi Okimoto and 2 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2022. 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
1.2field-weighted citation impact, top 24% 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, 12 citations in OpenAlex.

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  2. Loss ofCurrent issues in molecular biology · 2025
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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

12 authors at 9 institutions in 2 countries.

Hironao NakayamaDepartment of Medical Science and Technology, Hiroshima International University, Higashi-hiroshima, Hiroshima, 739-2695, Japan. Electronic address: hironao@hirokoku-u.ac.jp.
Hidetaka OhnukiLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Masako NakaharaDepartment of Medical Science and Technology, Hiroshima International University, Higashi-hiroshima, Hiroshima, 739-2695, Japan.
Hisayo Nishida-FukudaDepartment of Genome Editing, Institute of Biomedical Science, Kansai Medical University, Hirakata, Osaka, 5731010, Japan.
Tomohisa SakaueDivision of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Toon, Shitsukawa, Ehime, 791-0295, Japan; Department of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Shitsukawa, Ehime, 791-0295, Japan.
Shinji FukudaDivision of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Toon, Shitsukawa, Ehime, 791-0295, Japan; Department of Biochemistry, School of Dentistry, Aichi Gakuin University, Nagoya, Aichi, 464-8650, Japan.
Shigeki HigashiyamaDivision of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Toon, Shitsukawa, Ehime, 791-0295, Japan; Department of Molecular and Cellular Biology, Osaka International Cancer Institute, Chuo-ku, Osaka, 541-8567, Japan.
Yuki DoiDepartment of Surgery, Nippon Kokan Fukuyama Hospital, Fukuyama, Hiroshima, 721-0927, Japan.
Masahiro MitsuyoshiDepartment of Surgery, Nippon Kokan Fukuyama Hospital, Fukuyama, Hiroshima, 721-0927, Japan; Department of Surgery I, School of Medicine, University of Occupational and Environmental Health, Kita-kyushu, Fukuoka, 807-0804, Japan.
Takashi OkimotoDepartment of Surgery, Nippon Kokan Fukuyama Hospital, Fukuyama, Hiroshima, 721-0927, Japan; Department of Surgery, Kyushu Rosai Hospital, Kita-kyushu, Fukuoka, 800-0296, Japan.
Giovanna TosatoLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Chiaki KusumotoDepartment of Medical Science and Technology, Hiroshima International University, Higashi-hiroshima, Hiroshima, 739-2695, Japan; Department of Gastroenterology, Nippon Kokan Fukuyama Hospital, Fukuyama, Hiroshima, 721-0927, Japan. Electronic address: kusumoto@hirokoku-u.ac.jp.
Fukuyama Cardiovascular Hospital · JPHiroshima International University · JPNational Institutes of Health · USAichi Gakuin University · JPEhime University · JPKansai Medical University · JPKyushu Rosai Hospital · JPOsaka International Cancer Institute · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

Angiogenesis and Tumor GrowthZIASC010355 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI TOSATO, GIOVANNA · 2009 to 2025
$13.3M
Study of the Roles of SDF1 and CXCR4 in HematopoiesisZIABC010782 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TOSATO, GIOVANNA · 2009 to 2025
$10.2M
Intramural NIH HHS ZIA SC010355
6 · The paper itself

Abstract

Netrin-1, the protein product of the NTN1 gene, is an axon guidance molecule implicated in regulation of cell survival and tumorigenesis. Expression of the netrin-1 receptors deleted in colorectal cancer (DCC) and uncoordinated 5 homolog (UNC5H) is frequently silenced in colorectal cancer (CRC) by either loss of heterozygosity or epigenetic mechanisms. However, netrin-1 expression and regulation in CRC are mostly unknown. Here, we report that NTN1 expression is significantly reduced in most CRC tissues compared to the adjacent normal intestinal mucosa, and that NTN1 DNA methylation is significantly higher in CRCs (24.6%) than in the adjacent normal intestinal mucosa (4.0%). In 6 CRC cell lines, NTN1 expression is low. Treatment with 5-Aza-2'-deoxycytidine increased expression of NTN1 in CRC cell lines, indicating that DNA methylation represses NTN1 transcription in CRCs. NTN1 DNA hypermethylation was significantly associated with advanced CRC disease. Median netrin-1 serum levels were significantly decreased in CRC patients (330.1 pg/mL) compared with normal individuals (438.6 pg/mL). Our results suggest that netrin-1 is a candidate biomarker for CRC.

Indexed as

Colorectal NeoplasmsEpigenesis, GeneticNetrin-1Axon GuidanceHumansNetrin ReceptorsNetrin-1Netrin ReceptorsNTN1 protein, humanAxon guidanceColorectal cancerDNA methylationNetrin-1VEGF-A

Identifiers

PMID35489200
PMCPMC9155250
OpenAlexW4224272731

What OpenQuestion holds

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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.