Evidence map›Paper›PMID 27926503›Full record

ArticleOncotarget2017

FOXD3 is a tumor suppressor of colon cancer by inhibiting EGFR-Ras-Raf-MEK-ERK signal pathway.

Kun Li, Qunfeng Guo, Jun Yang, Hui Chen, Kewen Hu, Juan Zhao, Shunxin Zheng, Xiufeng Pang, Sufang Zhou, Yongyan Dang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

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  20. Cancer cell international · 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

11 authors at 3 institutions in 1 country.

Kun LiDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, Nanning, Guangxi, China.
Qunfeng GuoDepartment of Orthopedics, Changzheng Hospital, The Second Military Medical University, Shanghai, People's Republic of China.
Jun YangDepartment of Orthopedics, Changzheng Hospital, The Second Military Medical University, Shanghai, People's Republic of China.
Hui ChenShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Kewen HuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, China.
Juan ZhaoDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, Nanning, Guangxi, China.
Shunxin ZhengDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, Nanning, Guangxi, China.
Xiufeng PangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Sufang ZhouDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, Nanning, Guangxi, China.
Yongyan DangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Lei LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
East China Normal University · CNGuangxi Medical University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forkhead box D3 (FOXD3), as a transcriptional repressor, is well known to be involved in the regulation of development. Although FoxD3 is associated with several cancers, its role in colon cancer and the underlying mechanism are still unclear. Here, we first showed that FOXD3 knockdown dramatically increased the proliferation of human colon cancer cells, enhanced cell invasive ability and inhibited cell apoptosis. In vivo xenograft studies confirmed that the FOXD3-knockdown cells were more tumorigenic than the controls. Silencing FOXD3 markedly activated EGFR/Ras/Raf/MEK/ERK pathway in human colon cancer cells. In addition, blocking EGFR effectively decreased the activity of MAPK induced by FOXD3 knockdown. In human cancer tissue, the expression of FOXD3 was reduced, however, the EGFR/Ras/Raf/MEK/ERK pathway was activated. Our study indicates that FOXD3 may play a protective role in human colon formation by regulating EGFR/Ras/Raf/MEK/ERK signal pathway. It is proposed that FOXD3 may have potential as a new therapeutic target in human colon cancer treatment.

Indexed as

Down-RegulationAnimalsCaco-2 CellsCell ProliferationColonic NeoplasmsErbB ReceptorsFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHCT116 CellsHumansMAP Kinase Signaling SystemMiceMitogen-Activated Protein Kinase KinasesNeoplasm Transplantationraf KinasesEGFR protein, humanErbB ReceptorsForkhead Transcription FactorsFOXD3 protein, humanMitogen-Activated Protein Kinase Kinasesraf Kinasesras Proteinscolon cancerEGFRFOXD3Ras/Raf/MEK/ERK signal pathway

Identifiers

PMID27926503
PMCPMC5354891
OpenAlexW2560510548

What OpenQuestion holds

Textmetadata
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.