Evidence map›Paper›PMID 26183471›Full record

ArticleCancer science2015

FGF-1/-3/FGFR4 signaling in cancer-associated fibroblasts promotes tumor progression in colon cancer through Erk and MMP-7.

Yu-Pan Bai, Kun Shang, Huan Chen, Fei Ding, Zhen Wang, Chen Liang, Ye Xu, Meng-Hong Sun, Ying-Yi Li

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

71 citing papers in PubMed, 108 citations in OpenAlex.

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11 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Yu-Pan BaiCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Kun ShangCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Huan ChenDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Fei DingDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhen WangCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Chen LiangCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Ye XuDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Meng-Hong SunDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Ying-Yi LiCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs), as the activated fibroblasts in the tumor stroma, are important modifiers of tumour progression. In the present study, we observed that azoxymethane and dextran sodium sulfate treatments induced increasingly severe colorectal mucosal inflammation and the intratumoural accumulation of CAFs. Fibroblast growth factor (FGF)-1 and FGF-3 were detected in infiltrating cells, and FGFR4, the specific receptor for FGF-1 and FGF-3, was detected in colon cancer tissues. The phosphorylation of FGFR4 enhanced the production of metalloproteinase (MMP)-7 and mitogen-activated protein kinase kinase (Mek)/extracellular signal-regulated kinase (Erk), which was accompanied by excessive vessel generation and cell proliferation. Moreover, we separated CAFs, pericarcinoma fibroblasts (PFs), and normal fibroblasts (NFs) from human colon tissue specimens to characterize the function of CAFs. We observed that CAFs secrete more FGF-1/-3 than NFs and PFs and promote cancer cell growth and angiogenesis through the activation of FGFR4, which is followed by the activation of Mek/Erk and the modulation of MMP-7 expression. The administration of FGF-1/-3-neutralizing antibodies or the treatment of cells with FGFR4 siRNA or the FGFR4 inhibitor PD173074 markedly suppressed colon cancer cell proliferation and neovascularization. These observations suggest a crucial role for CAFs and FGF signaling in the initiation and progression of colorectal cancer. The inhibition of the FGF signaling pathway may be a useful strategy for the treatment of colon cancer.

Indexed as

AnimalsAzoxymethaneCell Line, TumorColitis, UlcerativeColonic NeoplasmsDextran SulfateDisease Models, AnimalDisease ProgressionExtracellular Signal-Regulated MAP KinasesFibroblast Growth Factor 1Fibroblast Growth Factor 3FibroblastsHCT116 CellsHT29 CellsHumansHuman Umbilical Vein Endothelial CellsAzoxymethaneDextran SulfateExtracellular Signal-Regulated MAP KinasesFGF3 protein, humanFGFR4 protein, humanFibroblast Growth Factor 1Fibroblast Growth Factor 3Matrix Metalloproteinase 7MMP7 protein, humanPD 173074PyrimidinesReceptor, Fibroblast Growth Factor, Type 4Receptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth FactorRNA, Small InterferingCancer-associated fibroblastscolon cancerextracellular signal-regulated kinasefibroblast growth factormetalloproteinase-7

Identifiers

PMID26183471
PMCPMC4637995
OpenAlexW1907149477

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.