Evidence map›Paper›PMID 27512995›Full record

ArticlePloS one2016

Thrombomodulin Influences the Survival of Patients with Non-Metastatic Colorectal Cancer through Epithelial-To-Mesenchymal Transition (EMT).

Yu-Jia Chang, Ya-Wen Cheng, Ruo-Kai Lin, Chi-Chou Huang, William Tzu-Liang Chen, Tao-Wei Ke, Po-Li Wei

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

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  13. Thrombomodulin Regulation of Mitogen-Activated Protein Kinases.International journal of molecular sciences · 2019
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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

7 authors at 4 institutions in 1 country.

Yu-Jia ChangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, ROC.
Ya-Wen ChengGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology,Taipei Medical University, Taipei, Taiwan, ROC.
Ruo-Kai LinGraduate Institute of Pharmacognosy, Taipei Medical University, Taipei, Taiwan, ROC.
Chi-Chou HuangSchool of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC.
William Tzu-Liang ChenDivision of Colorectal Surgery, Department of Surgery, China Medical University Hospital, Taichung, Taiwan, ROC.
Tao-Wei KeDivision of Colorectal Surgery, Department of Surgery, China Medical University Hospital, Taichung, Taiwan, ROC.
Po-Li WeiGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology,Taipei Medical University, Taipei, Taiwan, ROC.
Taipei Medical University · TWChina Medical University Hospital · TWChung Shan Medical University · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTreatment resistance and metastasis are the major causes of death among patients with colorectal cancer (CRC). Approximately 20% of surgically treated patients ultimately develop metastases during the follow-up period. Currently, the TNM system is the only available prognostic test. Therefore, the identification of new markers for CRC remains important. Thrombomodulin (TM), a glycoprotein, is involved in angiogenesis and has been linked to many malignant diseases. However, the function of TM in CRC remains unclear.

methodsA total of 170 patients with CRC participated in this study. TM expression was analyzed via immunohistochemistry. Univariate (Kaplan-Meier) analysis was used to analyze patient outcomes, including overall survival (OS) and disease-free survival (DFS). TM expression was manipulated using shRNA or an overexpression system. Transwell migration assays, wound healing migration assays, and the xCELLigence biosensor system were used to detect cell proliferative and migratory capacities.

resultsTM expression in the tumor tissues significantly and positively correlated with the DFS and OS of non-metastatic patients with CRC (ps = 0.036 and 0.0218, respectively). Suppression of TM expression increased the proliferation and migration of DLD-1 cells. TM overexpression reduced the cells' proliferative and migratory capacities. Cyclooxygenase (COX)-2 expression was up-regulated following TM silencing. Furthermore, the association between the migration of colon cancer cells and the levels of TM and epithelial-to-mesenchymal transition (EMT) markers (fibronectin, vimentin and ezrin) was confirmed in HT29 and DLD-1 cells.

conclusionsOur study demonstrates that patients with non-metastatic CRC display low TM expression in their tumors and exhibit reduced DFS and OS. The enhanced expression of mesenchymal markers and COX-2 may be involved in the mechanisms that underlie recurrence in patients with cancer displaying low TM expression.

Indexed as

Epithelial-Mesenchymal TransitionBiomarkers, TumorCell MovementCell ProliferationColorectal NeoplasmsCyclooxygenase 2Disease-Free SurvivalHumansPrognosisSurvival AnalysisThrombomodulinTumor Cells, CulturedUp-RegulationBiomarkers, TumorCyclooxygenase 2Thrombomodulin

Identifiers

PMID27512995
PMCPMC4981396
OpenAlexW2515690220

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.