Evidence map›Paper›PMID 26976794›Full record

ArticleScientific reports2016

Suppression of Spry1 inhibits triple-negative breast cancer malignancy by decreasing EGF/EGFR mediated mesenchymal phenotype.

Qing He, Hongyu Jing, Lucy Liaw, Lindsey Gower, Calvin Vary, Shucheng Hua, Xuehui Yang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
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  9. Article
  10. Review
  11. RASAL2 Confers Collateral MEK/EGFR Dependency in Chemoresistant Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Loss of Spry1 reduces growth of BRAFCell death & disease · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Qing HeCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Hongyu JingCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Lucy LiawCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Lindsey GowerCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Calvin VaryCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Shucheng HuaDepartment of Respiratory Medicine, The First Hospital of Jinlin University, Changchun, China.
Xuehui YangCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA.
Maine Medical Center · USMaine Medical Center Research Institute · USFirst Hospital of Jilin University · CNJilin University · CN

Funding

Progenitor Cell Analysis CoreP30GM106391 · NIGMS · MAINEHEALTH · PI WOJCHOWSKI, DON MICHAEL · 2013 to 2017
$5.7M
Phase III COBRE in Vascular BiologyP30GM103392 · NIGMS · MAINEHEALTH · PI ST. GERMAIN, DONALD L. · 2012 to 2016
$4.7M
NIGMS NIH HHS P30 GM1033465NIGMS NIH HHS P30 GM103392NIGMS NIH HHS P30 GM106391
6 · The paper itself

Abstract

Sprouty (Spry) proteins have been implicated in cancer progression, but their role in triple-negative breast cancer (TNBC), a subtype of lethal and aggressive breast cancer, is unknown. Here, we reported that Spry1 is significantly expressed in TNBC specimen and MDA-MB-231 cells. To understand Spry1 regulation of signaling events controlling breast cancer phenotype, we used lentiviral delivery of human Spry1 shRNAs to suppress Spry1 expression in MDA-MB-231, an established TNBC cell line. Spry1 knockdown MDA-MB-231 cells displayed an epithelial phenotype with increased membrane E-cadherin expression. Knockdown of Spry1 impaired MDA-MB-231 cell migration, Matrigel invasion, and anchorage-dependent and -independent growth. Tumor xenografts originating from Spry1 knockdown MDA-MB-231 cells grew slower, had increased E-cadherin expression, and yielded fewer lung metastases compared to control. Furthermore, suppressing Spry1 in MDA-MB-231 cells impaired the induction of Snail and Slug expression by EGF, and this effect was associated with increased EGFR degradation and decreased EGFR/Grb2/Shp2/Gab1 signaling complex formation. The same phenotype was also observed in the TNBC cell line MDA-MB-157. Together, our results show that unlike in some tumors, where Spry may mediate tumor suppression, Spry1 plays a selective role in at least a subset of TNBC to promote the malignant phenotype via enhancing EGF-mediated mesenchymal phenotype.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell Line, TumorCell MovementCell ProliferationCollagenDrug CombinationsEpidermal Growth FactorErbB ReceptorsFemaleGene Knockdown TechniquesHumansLamininMembrane ProteinsMice, Inbred NODMice, SCIDCollagenDrug CombinationsEpidermal Growth FactorErbB ReceptorsLamininmatrigelMembrane ProteinsPhosphoproteinsProteoglycansSPRY1 protein, human

Identifiers

PMID26976794
PMCPMC4791662
OpenAlexW2299966973

What OpenQuestion holds

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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.