Evidence map›Paper›PMID 31705019›Full record

ArticleScientific reports2019

Reduced RhoA expression enhances breast cancer metastasis with a concomitant increase in CCR5 and CXCR4 chemokines signaling.

Gardiyawasam Kalpana, Christopher Figy, Miranda Yeung, Kam C Yeung

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.8field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Review
  5. Review
  6. Functions of RhoA in the female reproductive system.Reproductive and developmental medicine · 2025
    Review
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  12. Cancers · 2024
    Review
  13. Article
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  17. Endocytosis in cancer and cancer therapy.Nature reviews. Cancer · 2023
    Review
  18. Review
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Gardiyawasam KalpanaDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio, 43614, USA.
Christopher FigyDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio, 43614, USA.
Miranda YeungDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio, 43614, USA.
Kam C YeungDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio, 43614, USA. kam.yeung@utoledo.edu.
University of Toledo · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of RhoA GTPases in breast cancer tumorigenesis and metastasis is unclear. Early studies within which mutations in RhoA were designed based on cancer-associated mutations in Ras supported an oncogene role for RhoA. However, recent whole-genome sequencing studies of cancers raised the possibility that RhoA may have a tumor suppression function. Here, using a syngeneic triple negative breast cancer murine model we investigated the physiological effects of reduced RhoA expression on breast cancer tumorigenesis and metastasis. RhoA knockdown had no effect on primary tumor formation and tumor proliferation, concurring with our in vitro findings where reduced RhoA had no effect on breast cancer cell proliferation and clonogenic growth. In contrast, primary tumors with RhoA knockdown efficiently invaded sentinel lymph nodes and significantly metastasized to lungs compared to control tumors. Mechanistically, the current study demonstrated that this is achieved by promoting a pro-tumor microenvironment, with increased cancer-associated fibroblasts and macrophage infiltration, and by modulating the CCL5-CCR5 and CXCL12-CXCR4 chemokine axes in the primary tumor. To our knowledge, this is the first such mechanistic study in breast cancer showing the ability of RhoA to suppress chemokine receptor expression in breast tumor cells. Our work suggests a physiological lung and lymph node metastasis suppressor role for RhoA GTPase in breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationFemaleHumansLung NeoplasmsMiceReceptors, CCR5Receptors, CXCR4rhoA GTP-Binding ProteinSignal TransductionTumor Cells, CulturedXenograft Model Antitumor AssaysBiomarkers, TumorCCR5 protein, humanCXCR4 protein, humanReceptors, CCR5Receptors, CXCR4rhoA GTP-Binding ProteinRHOA protein, human

Identifiers

PMID31705019
PMCPMC6841971
OpenAlexW2989138019

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.