Evidence map›Paper›PMID 24317509›Full record

ArticleOncogene2014

A critical role of CD29 and CD49f in mediating metastasis for cancer-initiating cells isolated from a Brca1-associated mouse model of breast cancer.

A Vassilopoulos, C Chisholm, T Lahusen, H Zheng, C-X Deng

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Structure, function and usage of integrin alpha 6 (CD49f): A comprehensive review.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2026
    Review
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  12. MicroRNA Regulation of Breast Cancer Stemness.International journal of molecular sciences · 2021
    Review
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  19. Hydrodynamic shear-based purification of cancer cells with enhanced tumorigenic potential.Integrative biology : quantitative biosciences from nano to macro · 2020
    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

5 authors at 2 institutions in 1 country.

A VassilopoulosGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, USA.
C ChisholmGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, USA.
T LahusenGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, USA.
H ZhengGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, USA.
C-X DengGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNorthwestern University · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Cancer metastasis is a lethal problem that claims the lives of over 90% of cancer patients. In this study, we have investigated metastatic potential of cancer stem cells (CSCs) isolated from mammary tumors of a Brca1-mutant mouse model. Our data indicated that CSCs, which are enriched in CD24(+)CD29(+)/CD49f(+) cell population, displayed much higher migration ability than CD24(-)CD29(-)/CD49f(-) cells in tissue culture and enhanced metastatic potential in allograft-nude mice. CD24(+)CD29(+) cells maintained the ability to differentiate and reconstitute heterogeneity in the metastatic tumors whereas CD24(-)CD29(-) cells could not. Corresponding to their enhanced metastatic ability, CD24(+)CD29(+) cells exhibited features of the epithelial to mesenchymal transition. Finally, using short hairpin RNA to knock down CD29 and/or CD49f in metastatic cancer cells, we demonstrated that while acute knockdown of CD29 or CD49f alone slightly decreased cell migration ability, knockdown of both genes generated a profound effect to block their migration, revealing an overlapping, yet critical function of both genes in the migration of CSCs. Our findings indicate that in addition to serving as markers of CSCs, CD29 and CD49f may also serve as potential therapeutic targets for cancer metastasis.

Indexed as

AnimalsBiomarkers, TumorBRCA1 ProteinCD24 AntigenCell MovementCells, CulturedDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticIntegrin alpha6Mammary Neoplasms, AnimalMammary Neoplasms, ExperimentalMice, NudeMutationNeoplastic Stem CellsBiomarkers, TumorBRCA1 ProteinCD24 AntigenCd24a protein, mouseIntegrin alpha6leptin receptor, mouseReceptors, Leptin

Identifiers

PMID24317509
OpenAlexW2018047723

What OpenQuestion holds

Textmetadata
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.