Evidence map›Paper›PMID 28938607›Full record

ArticleOncotarget2017

HGFL-mediated RON signaling supports breast cancer stem cell phenotypes via activation of non-canonical β-catenin signaling.

Sasha J Ruiz-Torres, Nancy M Benight, Rebekah A Karns, Elyse E Lower, Jun-Lin Guan, Susan E Waltz

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. Article
  6. Review
  7. RON (Cancers · 2022
    Article
  8. Review
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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

6 authors at 4 institutions in 1 country.

Sasha J Ruiz-TorresDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Nancy M BenightDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Rebekah A KarnsDivision of Bioinformatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Elyse E LowerDepartment of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Susan E WaltzDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · USVeterans Health Administration · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI LEE ARMISTEAD DENSON · 2007 to 2026
$24.4M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Ron Receptor Tyrosine Kinase Signaling in Breast CancerI01BX000803 · VA · CINCINNATI VA MEDICAL CENTER RESEARCH · PI WALTZ, SUSAN E · 2011 to 2025
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BLRD VA I01 BX000803NCI NIH HHS T32 CA117846NIDDK NIH HHS P30 DK078392
6 · The paper itself

Abstract

Breast cancer stem cells (BCSCs), which drive tumor progression, recurrence, and metastasis, are considered a major challenge for breast cancer treatments, thus the discovery of novel pathways regulating BCSC maintenance remains essential to develop new strategies to effectively target this population and combat disease mortality. The HGFL-RON signaling is overexpressed in human breast cancers and is associated with increased breast cancer progression, metastasis, and poor prognosis. Here, we report that overexpression of RON/MST1R and HGFL/MST1 in cell lines and primary tumors increases BCSC self-renewal, numbers, and tumorigenic potential after syngeneic transplantation. Transcriptome analyses also reveal that the HGFL-RON signaling pathway regulates additional BCSC functions and supports an immunosuppressive microenvironment to stimulate tumor formation and progression. Moreover, we show that genetic and chemical downregulation of HGFL-RON signaling disrupts BCSC phenotypes and tumor growth by suppressing the RON-mediated phosphorylation/activation of β-CATENIN/CTNNB1 and its effector NF-κB/RELA. These studies indicate that HGFL-RON signaling regulates BCSC phenotypes and the tumor microenvironment to drive tumorigenesis and present HGFL/RON as novel therapeutic targets to effectively eradicate BCSCs in patients.

Indexed as

breast cancerbreast cancer stem cellsHGFLRON receptor tyrosine kinaseβ-CATENIN

Identifiers

PMID28938607
PMCPMC5601703
OpenAlexW2738121247

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.