Evidence map›Paper›PMID 24550834›Full record

ArticleFrontiers in physiology2014

Semaphorin7A promotes tumor growth and exerts a pro-angiogenic effect in macrophages of mammary tumor-bearing mice.

Ramon Garcia-Areas, Stephania Libreros, Samantha Amat, Patricia Keating, Roberto Carrio, Phillip Robinson, Clifford Blieden, Vijaya Iragavarapu-Charyulu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

43 citing papers in PubMed, 67 citations in OpenAlex.

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  12. Pan-Cancer Analysis of the Prognostic and Immunological Role of SEMA7A.International journal of general medicine · 2024
    Article
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  20. Macphatics and PoEMs in Postpartum Mammary Development and Tumor Progression.Journal of mammary gland biology and neoplasia · 2020
    Review
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

8 authors at 2 institutions in 1 country.

Ramon Garcia-AreasTumor Immunology, Department of Biomedical Sciences, Florida Atlantic University Boca Raton, FL, USA.
Stephania LibrerosTumor Immunology, Department of Biomedical Sciences, Florida Atlantic University Boca Raton, FL, USA.
Samantha AmatTumor Immunology, Department of Biomedical Sciences, Florida Atlantic University Boca Raton, FL, USA.
Patricia KeatingImmunology, Department of Biological Sciences, Florida Atlantic University Boca Raton, FL, USA.
Roberto CarrioTumor Immunology, Microbiology and Immunology, University of Miami Miller School of Medicine Miami, FL, USA.
Phillip RobinsonDepartment of Clinical Sciences, Florida Atlantic University Boca Raton, FL, USA.
Clifford BliedenDepartment of Pathology and Laboratory Medicine, Jackson Memorial Hospital, University of Miami Miller School of Medicine Miami, FL, USA.
Vijaya Iragavarapu-CharyuluTumor Immunology, Department of Biomedical Sciences, Florida Atlantic University Boca Raton, FL, USA.
Florida Atlantic University · USUniversity of Miami · US

Funding

Role of CHI3L1 in accelerating breast cancer metastasis: a mechanistic approachR15CA135513 · NCI · FLORIDA ATLANTIC UNIVERSITY · PI IRAGAVARAPU-CHARYULU, VIJAYA L · 2008 to 2013
$904k
NCI NIH HHS R15 CA135513
6 · The paper itself

Abstract

Semaphorins are a large family of molecules involved in axonal guidance during the development of the nervous system and have been recently shown to have both angiogenic and anti-angiogenic properties. Specifically, semaphorin 7A (SEMA7A) has been reported to have a chemotactic activity in neurogenesis and to be an immune modulator through α1β1integrins. SEMA7A has been shown to promote monocyte chemotaxis and induce them to produce proinflammatory mediators. In this study we explored the role of SEMA7A in a murine model of breast cancer. We show that SEMA7A is highly expressed by DA-3 murine mammary tumor cells in comparison to normal mammary cells (EpH4), and that peritoneal elicited macrophages from mammary tumor-bearing mice also express SEMA7A at higher levels compared to those derived from normal mice. We also show that murine macrophages treated with recombinant murine SEMA7A significantly increased their expression of proangiogenic molecule CXCL2/MIP-2. Gene silencing of SEMA7A in peritoneal elicited macrophages from DA-3 tumor-bearing mice resulted in decreased CXCL2/MIP-2 expression. Mice implanted with SEMA7A silenced tumor cells showed decreased angiogenesis in the tumors compared to the wild type tumors. Furthermore, peritoneal elicited macrophages from mice bearing SEMA7A-silenced tumors produce significantly (p < 0.01) lower levels of angiogenic proteins, such as CXCL2/MIP-2, CXCL1, and MMP-9, compared to those from control DA-3 mammary tumors. We postulate that SEMA7A in mammary carcinomas may skew monocytes into a pro-tumorigenic phenotype to support tumor growth. SEMA7A could prove to be valuable in establishing new research avenues toward unraveling important tumor-host immune interactions in breast cancer patients.

Indexed as

angiogenesisbreast cancerCXCL2/MIP-2macrophagesMMP-9SEMA7A

Identifiers

PMID24550834
PMCPMC3914020
OpenAlexW2124506933

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.