Evidence map›Paper›PMID 33007133›Full record

ArticleCancer science2020

CD109 regulates in vivo tumor invasion in lung adenocarcinoma through TGF-β signaling.

Tetsuro Taki, Yukihiro Shiraki, Atsushi Enomoto, Liang Weng, Chen Chen, Naoya Asai, Yoshiki Murakumo, Kohei Yokoi, Masahide Takahashi, Shinji Mii

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Sexually distinct multi-omic responses to progressive endurance exercise training in the rat lung.American journal of respiratory cell and molecular biology · 2026
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  16. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review
  17. Article
  18. Article
  19. Article
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.

Tetsuro TakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0001-8654-6896
Yukihiro ShirakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-9206-6116
Liang WengDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Chen ChenDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Naoya AsaiDepartment of Molecular Pathology, Graduate School of Medicine, Fujita Health University, Toyoake, Japan.
Yoshiki MurakumoDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Japan.ORCID https://orcid.org/0000-0003-2843-8189
Kohei YokoiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahide TakahashiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shinji MiiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0001-8266-3235
Nagoya University · JPFujita Health University · JPKitasato University · JP

Funding

Chukyo Longevity Medical and Promotion FoundationJSPS KAKENHI 19K07503JSPS KAKENHI 26221304
6 · The paper itself

Abstract

Stromal invasion is considered an important prognostic factor in patients with lung adenocarcinoma. The mechanisms underlying the formation of tumor stroma and stromal invasion have been studied in the lung; however, they are still unclear. CD109 is a glycosylphosphatidylinositol-anchored glycoprotein highly expressed in several types of human malignant tumors including lung cancers. In this study, we investigated the in vivo functions of CD109 protein in malignant lung tumors. Initially, we identified an association between higher expression of CD109 protein in human lung adenocarcinoma and a significantly worse prognosis, according to immunohistochemical analysis. We also showed that CD109 deficiency significantly reduced the area of stromal invasive lesions in a genetically engineered CD109-deficient lung adenocarcinoma mouse model, which correlated with the results observed in human lung adenocarcinoma. Furthermore, we identified latent TGF-β binding protein-1 (LTBP1) as a CD109-interacting protein using mass spectrometry and confirmed their interaction by co-immunoprecipitation. Importantly, increased CD109 expression enhanced stromal TGF-β activation in the presence of LTBP1. Therefore, these data suggest the significance of the regulation of TGF-β signaling through CD109 and LTBP1 interaction in tumor stroma and also reveal the importance of CD109 expression levels in promoting lung cancer cell proliferation, migration, and invasion, and thus predicting the outcome of patients suffering from lung adenocarcinoma. Therefore, CD109 protein could be a potential therapeutic target for this disease.

Indexed as

AdenocarcinomaAgedAnimalsAntigens, CDCell Line, TumorCell MovementCell ProliferationClustered Regularly Interspaced Short Palindromic RepeatsDisease Models, AnimalFemaleGPI-Linked ProteinsHumansLatent TGF-beta Binding ProteinsLung NeoplasmsMaleMiceAntigens, CDCD109 protein, humanGPI-Linked ProteinsLatent TGF-beta Binding ProteinsLTBP1 protein, humanNeoplasm ProteinsRNA, Small InterferingTransforming Growth Factor betacarcinogenesisCD109LTBP1lung adenocarcinomamouse model

Identifiers

PMID33007133
PMCPMC7734007
OpenAlexW3090934714

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.