Evidence map›Paper›PMID 27132510›Full record

ArticleOncogene2016

Targeting TYRO3 inhibits epithelial-mesenchymal transition and increases drug sensitivity in colon cancer.

C-W Chien, P-C Hou, H-C Wu, Y-L Chang, S-C Lin, S-C Lin, B-W Lin, J-C Lee, Y-J Chang, H S Sun and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

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  18. Blocking antibody-mediated phosphatidylserine enhances cancer immunotherapy.Journal of cancer research and clinical oncology · 2021
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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 3 institutions in 1 country.

C-W ChienInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
P-C HouInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
H-C WuInstitute of Cellular and Organismic Biology, Academia Sinica, Nankang, Taipei, Taiwan.
Y-L ChangInstitute of Cellular and Organismic Biology, Academia Sinica, Nankang, Taipei, Taiwan.
S-C LinDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
S-C LinDepartment of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
B-W LinDepartment of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
J-C LeeDepartment of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Y-J ChangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
H S SunInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
S-J TsaiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TWInstitute of Cellular and Organismic Biology, Academia Sinica · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is the third leading cause of death from cancer worldwide with less than 10% survival rate at the late stage. Although mutations of certain genes have been implicated in familial colon cancer development, the etiology of the majority of colon cancer remains unknown. Herein, we identified TYRO3 as a potential oncogene. Immunohistochemical staining results demonstrated that levels of TYRO3 were markedly elevated in polyps and colon cancer cells and were negatively correlated with prognosis. Overexpression of TYRO3 enhanced cell motility, invasion, anchorage-independent growth and metastatic ability, while knockdown of TYRO3 impaired all these processes. Results from meta-analysis showed that TYRO3 was associated with epithelial-mesenchymal transition (EMT) signatures. Gain-of-function and loss-of-function experiments demonstrated that expression of SNAI1, the master regulator of EMT, was regulated by TYRO3 and played a major role in mediating TYRO3-induced EMT processes. The murine model also demonstrated that Tyro3 and Snai1 were upregulated in the early stage of colon cancer development. To provide a proof-of-concept that TYRO3 is a druggable target in colon cancer therapy, we raised anti-TYRO3 human antibodies and showed that treatment with the human antibody abolished TYRO3-induced EMT process. More importantly, administration of this anti-TYRO3 antibody increased drug sensitivity in primary cultured colon cancer cells and xenografted mouse tumors. These findings demonstrate that TYRO3 is a novel oncogene and a druggable target in colon cancer.

Indexed as

AnimalsCell Line, TumorCell Transformation, NeoplasticCluster AnalysisColonic NeoplasmsColonic PolypsDisease Models, AnimalDisease ProgressionDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene ExpressionGene Expression ProfilingGene Knockdown TechniquesHumansMaleMiceReceptor Protein-Tyrosine KinasesSNAI1 protein, humanSnail Family Transcription FactorsTYRO3 protein, human

Identifiers

PMID27132510
OpenAlexW2346898981

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.