Evidence map›Paper›PMID 26933086›Full record

ArticleCancer research2016

Rab11-FIP1C Is a Critical Negative Regulator in ErbB2-Mediated Mammary Tumor Progression.

Pierre-Luc Boulay, Louise Mitchell, Jason Turpin, Julie-Émilie Huot-Marchand, Cynthia Lavoie, Virginie Sanguin-Gendreau, Laura Jones, Shreya Mitra, Julie M Livingstone, Shirley Campbell and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. [miR-125b-5p inhibits proliferation and migration of osteosarcoma cells by negatively regulating RAB3D expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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  7. Review
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  9. Role of Rab GTPases in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021
    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

17 authors at 5 institutions in 3 countries.

Pierre-Luc BoulayDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Louise MitchellIntegrin Cell Biology Cancer Research UK Beaston Institute, Glasgow, United Kingdom.
Jason TurpinDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Julie-Émilie Huot-MarchandDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Cynthia LavoieDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Virginie Sanguin-GendreauDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Laura JonesDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Shreya MitraDepartment of System Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Julie M LivingstoneDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Shirley CampbellDepartment of Pharmacology, University of Montreal, Québec, Canada.
Michael HallettDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Gordon B MillsDepartment of System Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Morag ParkDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada.
Lewis ChodoshCancer Biology Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Douglas StrathdeeIntegrin Cell Biology Cancer Research UK Beaston Institute, Glasgow, United Kingdom.
Jim C NormanIntegrin Cell Biology Cancer Research UK Beaston Institute, Glasgow, United Kingdom.
William J MullerDepartment of Biochemistry, McGill University, Rosalind and Morris Goodman Cancer Research Montreal, Québec, Canada. william.muller@mcgill.ca.
McGill University · CACancer Research UK Scotland Institute · GBThe University of Texas MD Anderson Cancer Center · USCancer Support Community · USUniversité de Montréal · CA

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Tyrosine Kinase-Dependant and - Independent Pathways of EGFR in Breast Cancer ProP01CA099031 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2003 to 2014
$11.6M
Cancer Research UK 18277NCI NIH HHS P01 CA099031NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Rab coupling protein (FIP1C), an effector of the Rab11 GTPases, including Rab25, is amplified and overexpressed in 10% to 25% of primary breast cancers and correlates with poor clinical outcome. Rab25 is also frequently silenced in triple-negative breast cancer, suggesting its ability to function as either an oncogene or a tumor suppressor, depending on the breast cancer subtype. However, the pathobiologic role of FIP family members, such as FIP1C, in a tumor-specific setting remains elusive. In this study, we used ErbB2 mouse models of human breast cancer to investigate FIP1C function in tumorigenesis. Doxycycline-induced expression of FIP1C in the MMTV-ErbB2 mouse model resulted in delayed mammary tumor progression. Conversely, targeted deletion of FIP1C in the mammary epithelium of an ErbB2 model coexpressing Cre recombinase led to accelerated tumor onset. Genetic and biochemical characterization of these FIP1C-proficient and -deficient tumor models revealed that FIP1C regulated E-cadherin (CDH1) trafficking and ZONAB (YBX3) function in Cdk4-mediated cell-cycle progression. Furthermore, we demonstrate that FIP1C promoted lysosomal degradation of ErbB2. Consistent with our findings in the mouse, the expression of FIP1C was inversely correlated with ErbB2 levels in breast cancer patients. Taken together, our findings indicate that FIP1C acts as a tumor suppressor in the context of ErbB2-positive breast cancer and may be therapeutically exploited as an alternative strategy for targeting aberrant ErbB2 expression. Cancer Res; 76(9); 2662-74. ©2016 AACR.

Indexed as

AnimalsBreast NeoplasmsCell Transformation, NeoplasticDisease ProgressionErb-b2 Receptor Tyrosine KinasesFemaleFluorescent Antibody TechniqueHeterograftsHumansImmunoblottingMammary Neoplasms, ExperimentalMiceMice, Knockoutrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsERBB2 protein, humanErb-b2 Receptor Tyrosine Kinasesrab11 GTP-Binding Proteinsrab GTP-Binding Proteins

Identifiers

PMID26933086
PMCPMC5070470
OpenAlexW2290707026

What OpenQuestion holds

Textmetadata
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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.