Evidence map›Paper›PMID 30189360›Full record

ArticleNeoplasia (New York, N.Y.)2018

FOXF1 Induces Epithelial-Mesenchymal Transition in Colorectal Cancer Metastasis by Transcriptionally Activating SNAI1.

Shuyang Wang, Shanshan Yan, Shaowei Zhu, Yali Zhao, Junyu Yan, Zhiyuan Xiao, Jiaxin Bi, Junfeng Qiu, Dan Zhang, Zexuan Hong and 8 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 47 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

18 authors at 3 institutions in 1 country.

Shuyang WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Shanshan YanDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Shaowei ZhuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Yali ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Junyu YanDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Zhiyuan XiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Jiaxin BiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Junfeng QiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Dan ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Zexuan HongDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Lingjie ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Chengmei HuangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Tingting LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Li LiangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Wenting LiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Hongli JiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China. Electronic address: 25048195@qq.com.
Yanqing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China. Electronic address: dyq@fimmu.com.
Yaping YeDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China. Electronic address: 149941225@qq.com.
Key Laboratory of Guangdong Province · CNNanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forkhead Box F1 (FOXF1) has been recently implicated in cancer progression and metastasis of lung cancer and breast cancer. However, the biological functions and underlying mechanisms of FOXF1 in the regulation of the progression of colorectal cancer (CRC) are largely unknown. We showed that FOXF1 was up-regulated in 93 paraffin-embedded archived human CRC tissue, and both high expression and nuclear location of FOXF1 were significantly associated with the aggressive characteristics and poorer survival of CRC patients. The GSEA analysis showed that the higher level of FOXF1 was positively associated with an enrichment of EMT gene signatures, and exogenous overexpression of FOXF1 induced EMT by transcriptionally activating SNAI1. Exogenous overexpression FOXF1 functionally promoted invasion and metastasis features of CRC cells, and inhibition of SNAI1 attenuates the invasive phenotype and metastatic potential of FOXF1-overexpressing CRC cells. Furthermore, the results of the tissue chip showed that the expression of FOXF1 was positively correlated with SNAI1 in CRC tissues chip. These results suggested that FOXF1 plays a critical role in CRC metastasis by inducing EMT via transcriptional activation of SNAI1, highlighting a potential new therapeutic strategy for CRC.

Indexed as

AnimalsCell Line, TumorCell NucleusColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CSnail Family Transcription FactorsTranscriptional ActivationXenograft Model Antitumor AssaysForkhead Transcription FactorsFOXF1 protein, humanSNAI1 protein, humanSnail Family Transcription Factors

Identifiers

PMID30189360
PMCPMC6134153
OpenAlexW2890139621

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.