Evidence map›Paper›PMID 35831580›Full record

ArticleOncogene2022

Tumor cell-derived ANGPTL2 promotes β-catenin-driven intestinal tumorigenesis.

Haruki Horiguchi, Tsuyoshi Kadomatsu, Shinsei Yumoto, Takeshi Masuda, Keishi Miyata, Shuji Yamamura, Michio Sato, Jun Morinaga, Sumio Ohtsuki, Hideo Baba and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 11 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

12 authors at 2 institutions in 1 country.

Haruki HoriguchiDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.ORCID http://orcid.org/0000-0001-9344-8362
Tsuyoshi KadomatsuDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan. tkado@gpo.kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0003-3327-6954
Shinsei YumotoDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.
Takeshi MasudaDepartment of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.ORCID http://orcid.org/0000-0003-0121-4783
Keishi MiyataDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.
Shuji YamamuraDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.
Michio SatoDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.ORCID http://orcid.org/0000-0001-9339-1642
Jun MorinagaDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan.
Sumio OhtsukiDepartment of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.
Hideo BabaDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.
Toshiro MoroishiCenter for Metabolic Regulation of Healthy Aging (CMHA), Graduate School of Medical Sciences, Kumamoto University, Kumamoto, 860-8556, Japan.ORCID http://orcid.org/0000-0001-6419-3882
Yuichi OikeDepartment of Molecular Genetics, Graduate School of Medical Science, Kumamoto University, Kumamoto, 860-8556, Japan. oike@gpo.kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0003-3245-5395
Kumamoto University · JPKumamoto Health Science University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrolled proliferation of intestinal epithelial cells caused by mutations in genes of the WNT/β-catenin pathway is associated with development of intestinal cancers. We previously reported that intestinal stromal cell-derived angiopoietin-like protein 2 (ANGPTL2) controls epithelial regeneration and intestinal immune responses. However, the role of tumor cell-derived ANGPTL2 in intestinal tumorigenesis remained unclear. Here, we show that tumor cell-derived ANGPTL2 promotes β-catenin-driven intestinal tumorigenesis. ANGPTL2 deficiency suppressed intestinal tumor development in an experimental mouse model of sporadic colon cancer. We also found that increased ANGPTL2 expression in colorectal cancer (CRC) cells augments β-catenin pathway signaling and promotes tumor cell proliferation. Relevant to mechanism, our findings suggest that tumor cell-derived ANGPTL2 upregulates expression of OB-cadherin, which then interacts with β-catenin, blocking destruction complex-independent proteasomal degradation of β-catenin proteins. Moreover, our observations support a model whereby ANGPTL2-induced OB-cadherin expression in CRC cells is accompanied by decreased cell surface integrin α5β1 expression. These findings overall provide novel insight into mechanisms of β-catenin-driven intestinal tumorigenesis.

Indexed as

Colorectal NeoplasmsIntestinal NeoplasmsAngiopoietin-Like Protein 2Angiopoietin-like ProteinsAnimalsbeta CateninCarcinogenesisCell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticMiceWnt Signaling PathwayAngiopoietin-Like Protein 2Angiopoietin-like ProteinsAngptl2 protein, mousebeta Catenin

Identifiers

PMID35831580
OpenAlexW4285084371

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.