Evidence map›Paper›PMID 27764793›Full record

ArticleOncotarget2016

DcR3 induces epithelial-mesenchymal transition through activation of the TGF-β3/SMAD signaling pathway in CRC.

Yan-Ping Liu, Hui-Fang Zhu, Ding-Li Liu, Zhi-Yan Hu, Sheng-Nan Li, He-Ping Kan, Xiao-Yan Wang, Zu-Guo Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 20 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

8 authors at 2 institutions in 1 country.

Yan-Ping LiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hui-Fang ZhuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ding-Li LiuState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhi-Yan HuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Sheng-Nan LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
He-Ping KanDepartment of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiao-Yan WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zu-Guo LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decoy receptor 3 (DcR3), a novel member of the tumor necrosis factor receptor (TNFR) family, was recently reported to be associated with tumorigenesis and metastasis. However, the role of DcR3 in human colorectal cancer (CRC) has not been fully elucidated. In this study, we found that DcR3 expression was significantly higher in human colorectal cancer tissues than in paired normal tissues, and that DcR3 expression was strongly correlated with tumor invasion, lymph node metastases and poor prognoses. Moreover, DcR3 overexpression significantly enhanced CRC cell proliferation and migration in vitro and tumorigenesis in vivo. Conversely, DcR3 knockdown significantly repressed CRC cell proliferation and migration in vitro, and DcR3 deficiency also attenuated CRC tumorigenesis and metastasis in vivo. Functionally, DcR3 was essential for TGF-β3/SMAD-mediated epithelial-mesenchymal transition (EMT) of CRC cells. Importantly, cooperation between DcR3 and TGF-β3/SMAD-EMT signaling-related protein expression was correlated with survival and survival time in CRC patients. In conclusion, our results demonstrate that DcR3 may be a prognostic biomarker for CRC and that this receptor facilitates CRC development and metastasis by participating in TGF-β3/SMAD-mediated EMT of CRC cells.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMiceNeoplasm TransplantationPrognosisReceptors, Tumor Necrosis Factor, Member 6bSignal TransductionSmad ProteinsReceptors, Tumor Necrosis Factor, Member 6bSmad ProteinsTGFB3 protein, humanTNFRSF6B protein, humanTransforming Growth Factor beta3colorectal cancerdecoy receptor 3epithelial-mesenchymal transitionmetastasisTGF-β3/SMAD signaling

Identifiers

PMID27764793
PMCPMC5363587
OpenAlexW2531403772

What OpenQuestion holds

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LicenceCC BY
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.