Evidence map›Paper›PMID 36961882›Full record

ArticleOncotarget2023

Downregulation of angulin-1/LSR induces malignancy via upregulation of EGF-dependent claudin-2 and TGF-β-dependent cell metabolism in human lung adenocarcinoma A549 cells.

Wataru Arai, Takumi Konno, Takayuki Kohno, Yuki Kodera, Mitsuhiro Tsujiwaki, Yuma Shindo, Hirofumi Chiba, Masahiro Miyajima, Yuji Sakuma, Atsushi Watanabe and 1 more

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In one paragraph

Article in Oncotarget, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 7 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

11 authors at 1 institution in 1 country.

Wataru AraiDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takumi KonnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takayuki KohnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yuki KoderaDepartment of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Mitsuhiro TsujiwakiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yuma ShindoDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hirofumi ChibaDepartment of Respiratory Medicine and Allergology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masahiro MiyajimaDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yuji SakumaDepartment of Molecular Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Atsushi WatanabeDepartment of Thoracic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takashi KojimaDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal expression of bicellular tight junction claudins, including claudin-2 are observed during carcinogenesis in human lung adenocarcinoma. However, little is known about the role of tricellular tight junction molecule angulin-1/lipolysis-stimulated lipoprotein receptor (LSR). In the lung adenocarcinoma tissues examined in the present study, expression of claudin-2 was higher than in normal lung tissues, while angulin-1/LSR was poorly or faintly expressed. We investigated how loss of angulin-1/LSR affects the malignancy of lung adenocarcinoma cell line A549 and normal human lung epithelial (HLE) cells. The EGF receptor tyrosine kinase inhibitor AG1478 prevented the increase of claudin-2 expression induced by EGF in A549 cells. Knockdown of LSR induced expression of claudin-2 at the protein and mRNA levels and AG1478 prevented the upregulation of claudin-2 in A549 cells. Knockdown of LSR induced cell proliferation, cell migration and cell metabolism in A549 cells. Knockdown of claudin-2 inhibited the cell proliferation but did not affect the cell migration or cell metabolism of A549 cells. The TGF-β type I receptor inhibitor EW-7197 prevented the decrease of LSR and claudin-2 induced by TGF-β1 in A549 cells and 2D culture of normal HLE cells. EW-7197 prevented the increase of cell migration and cell metabolism induced by TGF-β1 in A549 cells. EW-7197 prevented the increase of epithelial permeability of FITC-4kD dextran induced by TGF-β1 in 2.5D culture of normal HLE cells. In conclusion, downregulation of angulin-1/LSR induces malignancy via EGF-dependent claudin-2 and TGF-β-dependent cell metabolism in human lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungLung NeoplasmsA549 CellsAniline CompoundsClaudin-2Down-RegulationEpidermal Growth FactorHumansQuinazolinesTight JunctionsTransforming Growth Factor betaTransforming Growth Factor beta1TriazolesTyrphostinsUp-RegulationAniline CompoundsClaudin-2Epidermal Growth FactorQuinazolinesRTKI cpdTransforming Growth Factor betaTransforming Growth Factor beta1TriazolesTyrphostinsvactosertibangulin-1/LSRcell metabolismclaudin-2lung adenocarcinomamalignancy

Identifiers

PMID36961882
PMCPMC10038356
OpenAlexW4360843640

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read79
identifiers read1
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.