Evidence map›Paper›PMID 22152016›Full record

ArticleBreast cancer research : BCR2011

Opposing roles of CXCR4 and CXCR7 in breast cancer metastasis.

Lorena Hernandez, Marco A O Magalhaes, Salvatore J Coniglio, John S Condeelis, Jeffrey E Segall

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 138 citations in OpenAlex.

  1. Review
  2. Incretin-Based Therapies and Cancer: What's New?Medicina (Kaunas, Lithuania) · 2025
    Review
  3. Review
  4. Article
  5. CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.International journal of biological sciences · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Lorena HernandezDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Marco A O Magalhaes
Salvatore J Coniglio
John S Condeelis
Jeffrey E Segall
Albert Einstein College of Medicine · US

Funding

Tumor Progression and MetastasisP01CA100324 · NCI · YESHIVA UNIVERSITY · PI CONDEELIS, JOHN S · 2003 to 2018
$30.0M
Characterization of the Invasion and Intravasation of Breast Cancer CellsF31CA110269 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HERNANDEZ-TELLEZ, LORENA · 2007 to 2009
$137k
NCI NIH HHS CA100324NCI NIH HHS CA110269
6 · The paper itself

Abstract

introductionCXCL12-CXCR4 signaling has been shown to play a role in breast cancer progression by enhancing tumor growth, angiogenesis, triggering cancer cell invasion in vitro, and guiding cancer cells to their sites of metastasis. However, CXCR7 also binds to CXCL12 and has been recently found to enhance lung and breast primary tumor growth, as well as metastasis formation. Our goal was to dissect the contributions of CXCR4 and CXCR7 to the different steps of metastasis - in vivo invasion, intravasation and metastasis formation.

methodsWe overexpressed CXCR4, CXCR7 or both in the rat mammary adenocarcinoma cell line MTLn3. Stable expressors were used to form tumors in severe combined immunodeficiency (SCID) mice, and in vivo invasiveness, intravital motility, intravasation, and metastasis were measured.

resultsWe found that CXCR4 overexpression increased the chemotactic and invasive behavior of MTLn3 cells to CXCL12, both in vitro and in vivo, as well as in vivo motility and intravasation. CXCR7 overexpression enhanced primary tumor growth and angiogenesis (as indicated by microvessel density and VEGFA expression), but decreased in vivo invasion, intravasation, and metastasis formation. In vitro, expression of CXCR7 alone had no effect in chemotaxis or invasion to CXCL12. However, in the context of increased CXCR4 expression, CXCR7 enhanced chemotaxis to CXCL12 but decreased invasion in response to CXCL12 in vitro and in vivo and impaired CXCL12 stimulated matrix degradation. The changes in matrix degradation correlated with expression of matrix metalloproteinase 12 (MMP12).

conclusionsWe find that CXCR4 and CXCR7 play different roles in metastasis, with CXCR4 mediating breast cancer invasion and CXCR7 impairing invasion but enhancing primary tumor growth through angiogenesis.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationChemokine CXCL12ChemotaxisFemaleGene ExpressionHumansMiceMice, SCIDNeoplasm MetastasisRatsReceptors, CXCRReceptors, CXCR4ACKR3 protein, humanChemokine CXCL12Receptors, CXCRReceptors, CXCR4

Identifiers

PMID22152016
PMCPMC3326570
OpenAlexW2140193755

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.