Evidence map›Paper›PMID 36739585›Full record

ArticleJournal of gastroenterology2023

LAT1 expression influences Paneth cell number and tumor development in Apc

Yunlong Sui, Namiko Hoshi, Ryuichi Ohgaki, Lingling Kong, Ryutaro Yoshida, Norihiro Okamoto, Masato Kinoshita, Haruka Miyazaki, Yuna Ku, Eri Tokunaga and 11 more

Erratum issuedOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 4 institutions in 3 countries.

Yunlong SuiDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Namiko HoshiDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan. nhoshi@med.kobe-u.ac.jp.ORCID http://orcid.org/0000-0003-2768-3991
Ryuichi OhgakiDepartment of Bio-system Pharmacology, Graduate School of Medicine, Osaka University, Osaka, 565-0871, Japan.
Lingling KongDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Ryutaro YoshidaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Norihiro OkamotoDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Masato KinoshitaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Haruka MiyazakiDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Yuna KuDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Eri TokunagaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Yuki ItoDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Daisuke WatanabeDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Makoto OoiDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Masakazu ShinoharaDivision of Molecular Epidemiology, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Kengo SasakiGraduate School of Science, Technology and Innovation, Kobe University, Hyogo, 657-8501, Japan.
Yoh ZenInstitute of Liver Studies, King's College Hospital, London, SE5 9RS, UK.
Takenori KotaniDivision of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Takashi MatozakiDivision of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Zibin TianDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Yoshikatsu KanaiDepartment of Bio-system Pharmacology, Graduate School of Medicine, Osaka University, Osaka, 565-0871, Japan.
Yuzo KodamaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.
Kobe University · JPThe University of Osaka · JPKing's College Hospital · GBQingdao University · CN

Funding

Japan Society for the Promotion of Science 19K08421Japan Society for the Promotion of Science 20H04123
6 · The paper itself

Abstract

backgroundAmino acid transporters play an important role in supplying nutrition to cells and are associated with cell proliferation. L-type amino acid transporter 1 (LAT1) is highly expressed in many types of cancers and promotes tumor growth; however, how LAT1 affects tumor development is not fully understood.

methodsTo investigate the role of LAT1 in intestinal tumorigenesis, mice carrying LAT1 floxed alleles that also expressed Cre recombinase from the promoter of gene encoding Villin were crossed to an Apc

resultsThis study showed that LAT1 was constitutively expressed in normal crypt base cells, and its conditional deletion in the intestinal epithelium resulted in fewer Paneth cells. LAT1 deletion reduced tumor size and number in the small intestine of Apc

conclusionsLAT1 affects intestinal tumor development in a cell-extrinsic manner through reduced Wnt3 expression in Paneth cells. Our findings may partly explain how nutrient availability can affect the risk of tumor development in the intestines.

Indexed as

Adenomatous Polyposis Coli ProteinAmino Acid Transport System y+LIntestinal NeoplasmsPaneth CellsAnimalsCell Transformation, NeoplasticIntestinal MucosaIntestinesIntestine, SmallMiceAdenomatous Polyposis Coli Proteinadenomatous polyposis coli protein, mouseAmino Acid Transport System y+LSlc7a7 protein, mouseCancerL-type amino acid transporter 1mTORC1Paneth cellsWnt3

Identifiers

PMID36739585
PMCPMC10140238
OpenAlexW4319262142

What OpenQuestion holds

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LicenceCC BY
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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.