Evidence map›Paper›PMID 32133706›Full record

ArticleCancer science2020

Elevation of CD109 promotes metastasis and drug resistance in lung cancer via activation of EGFR-AKT-mTOR signaling.

Kang-Yun Lee, Pei-Wei Shueng, Chih-Ming Chou, Bo-Xing Lin, Mei-Hsiang Lin, Deng-Yu Kuo, I-Lin Tsai, Sheng-Ming Wu, Cheng-Wei Lin

Abstract 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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. Article
  2. Antagonist nanobodies prevent protease inhibition by CD109.The Journal of biological chemistry · 2026
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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

9 authors.

Kang-Yun LeeDivision of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Pei-Wei ShuengDivision of Radiation Oncology, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Chih-Ming ChouDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Bo-Xing LinDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Mei-Hsiang LinGraduate Institute of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan.
Deng-Yu KuoDivision of Radiation Oncology, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
I-Lin TsaiDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Sheng-Ming WuDivision of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Cheng-Wei LinDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.ORCID https://orcid.org/0000-0003-4622-2680

Funding

Far Eastern Memorial Hospital FEMH-2019-C-013Taipei Medical University and Shuang Ho Hospital 106SHH-TMU-03The Ministry of Science and Technology, Taiwan MOST106-2320-B-038-040The Ministry of Science and Technology, Taiwan MOST107-2320-B-038-052-MY3
6 · The paper itself

Abstract

Lung cancer is the most commonly diagnosed cancer worldwide, and metastasis in lung cancer is the leading cause of cancer-related deaths. Thus, understanding the mechanism of lung cancer metastasis will improve the diagnosis and treatment of lung cancer patients. Herein, we found that expression of cluster of differentiation 109 (CD109) was correlated with the invasive and metastatic capacities of lung adenocarcinoma cells. CD109 is upregulated in tumorous tissues, and CD109 overexpression was associated with tumor progression, distant metastasis, and a poor prognosis in patient with lung adenocarcinoma. Mechanistically, expression of CD109 regulates protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling via its association with the epidermal growth factor receptor (EGFR). Inhibition of CD109 decreases EGFR phosphorylation, diminishes EGF-elicited activation of AKT/mTOR, and sensitizes tumor cells to an EGFR inhibitor. Taken together, our results show that CD109 is a potential diagnostic and therapeutic target in lung cancer patients.

Indexed as

Drug Resistance, NeoplasmA549 CellsAdenocarcinoma of LungAnimalsAntigens, CDBiomarkers, TumorCell Line, TumorCell ProliferationErbB ReceptorsGene ExpressionGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansLung NeoplasmsMiceMice, NudeAntigens, CDBiomarkers, TumorCD109 protein, humanEGFR protein, humanErbB ReceptorsGPI-Linked ProteinsMTOR protein, humanNeoplasm ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCD109EGFRlung cancermetastasismTOR

Identifiers

PMID32133706
PMCPMC7226182

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Registered trials

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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.