Evidence map›Paper›PMID 26485767›Full record

ArticleOncotarget2015

CXCR3 as a molecular target in breast cancer metastasis: inhibition of tumor cell migration and promotion of host anti-tumor immunity.

Guiquan Zhu, H Hannah Yan, Yanli Pang, Jiang Jian, Bhagelu R Achyut, Xinhua Liang, Jonathan M Weiss, Robert H Wiltrout, M Christine Hollander, Li Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

52 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  3. Artemis: Harnessing Knowledge Graphs for Next-Generation Drug Target Prioritization.Computational and structural biotechnology journal · 2026
    Article
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  14. Targeting CXCL9/10/11-CXCR3 axis: an important component of tumor-promoting and antitumor immunity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  15. Article
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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

10 authors at 3 institutions in 2 countries.

Guiquan ZhuLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
H Hannah YanLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Yanli PangLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Jiang JianLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Bhagelu R AchyutLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Xinhua LiangDepartment of Oral and Maxillofacial Surgery, State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, P. R. China.
Jonathan M WeissCancer and Inflammation Program, National Cancer Institute, Frederick, MD, USA.
Robert H WiltroutCancer and Inflammation Program, National Cancer Institute, Frederick, MD, USA.
M Christine HollanderLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Li YangLaboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD, USA.
National Cancer Institute · USPeking University · CNState Key Laboratory of Oral Diseases

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Chemokines and chemokine receptors have critical roles in cancer metastasis and have emerged as one of the targeting options in cancer therapy. However, the treatment efficacy on both tumor and host compartments needs to be carefully evaluated. Here we report that targeting CXCR3 decreased tumor cell migration and at the same time improved host anti-tumor immunity. We observed an increased expression of CXCR3 in metastatic tumor cells compared to those from non-metastatic tumor cells. Knockdown (KD) of CXCR3 in metastatic tumor cells suppressed tumor cell migration and metastasis. Importantly, CXCR3 expression in clinical breast cancer samples correlated with progression and metastasis. For the host compartment, deletion of CXCR3 in all host cells in 4T1 mammary tumor model significantly decreased metastasis. The underlying mechanisms involve a decreased expression of IL-4, IL-10, iNOs, and Arg-1 in myeloid cells and an increased T cell response. IFN-γ neutralization diminished the metastasis inhibition in the CXCR3 knockout (KO) mice bearing 4T1 tumors, suggesting a critical role of host CXCR3 in immune suppression. Consistently, targeting CXCR3 using a small molecular inhibitor (AMG487) significantly suppressed metastasis and improved host anti-tumor immunity. Our findings demonstrate that targeting CXCR3 is effective in both tumor and host compartments, and suggest that CXCR3 inhibition is likely to avoid adverse effects on host cells.

Indexed as

Cell MovementAnimalsBreast NeoplasmsCell Line, TumorCell SeparationFemaleFlow CytometryFluorescent Antibody TechniqueGene Knockdown TechniquesHumansMiceMice, Inbred BALB CMice, KnockoutNeoplasm InvasivenessPolymerase Chain ReactionReceptors, CXCR3Cxcr3 protein, mouseReceptors, CXCR3CXCR3drug treatmenthost immunitymigrationtumor metastasis

Identifiers

PMID26485767
PMCPMC4791240
OpenAlexW1811130292

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.