Evidence map›Paper›PMID 28455419›Full record

ArticleCancer research2017

CXCL1 Is Critical for Premetastatic Niche Formation and Metastasis in Colorectal Cancer.

Dingzhi Wang, Haiyan Sun, Jie Wei, Bo Cen, Raymond N DuBois

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

233 citing papers in PubMed, 359 citations in OpenAlex.

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  8. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    Review
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173 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

5 authors at 2 institutions in 1 country.

Dingzhi WangDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina.
Haiyan SunLaboratory for Inflammation and Cancer, Biodesign Institute of Arizona State University, Tempe, Arizona.
Jie WeiDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina.
Bo CenDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina.
Raymond N DuBoisDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina. duboisrn@musc.edu.
Medical University of South Carolina · USArizona State University · US

Funding

THE ROLE OF ENDOCANNABINOIDS AND THEIR RECEPTORS IN COLORECTAL CANCERP01CA077839 · NCI · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 1999 to 2016
$17.8M
Role of Eicosanoids in Intestinal BiologyR01DK047297 · NIDDK · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 1994 to 2018
$2.6M
(PQA1)The Molecular Mechanisms Underlying Effects of Aspirin on Colorectal CancerR01CA184820 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DUBOIS, RAYMOND N. · 2014 to 2017
$1.6M
NCI NIH HHS P01 CA077839NCI NIH HHS R01 CA184820NIDDK NIH HHS R01 DK047297
6 · The paper itself

Abstract

Emerging evidence suggests that the primary tumor influences the development of supportive metastatic microenvironments, referred to as premetastatic niches, in certain distant organs before arrival of metastatic cells. However, the mechanisms underlying the contributions of the primary tumor to premetastatic niche formation are not fully understood. Here, we demonstrate that colorectal carcinoma cells secrete VEGFA, which stimulates tumor-associated macrophages to produce CXCL1 in the primary tumor. Elevation of CXCL1 in premetastatic liver tissue recruited CXCR2-positive myeloid-derived suppressor cells (MDSC) to form a premetastatic niche that ultimately promoted liver metastases. Importantly, premetastatic liver-infiltrating MDSCs induced tumor cell survival without involvement of innate or adaptive immune responses. Our study provides the first evidence that primary malignant cell-secreted VEGFA stimulates tumor-associated macrophages to produce CXCL1, which recruits CXCR2-positive MDSCs to form a premetastatic niche to promote liver metastases. Our findings not only shed light on how the tumor microenvironment contributes to premetastatic niche formation at distant sites, but they also provide comprehensive insights into how MDSCs are recruited to other organs where they contribute to metastatic spread of disease. Moreover, our work also provides a rationale for development of CXCR2 antagonists to inhibit or prevent metastatic spread of disease.

Indexed as

AnimalsChemokine CXCL1Colorectal NeoplasmsHCT116 CellsHeterograftsHumansLiver NeoplasmsMaleMiceMice, Inbred NODMice, SCIDNeoplasm MetastasisNeoplastic Stem CellsStem Cell NicheTumor MicroenvironmentChemokine CXCL1CXCL1 protein, human

Identifiers

PMID28455419
PMCPMC5877403
OpenAlexW2608625783

What OpenQuestion holds

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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.