Evidence map›Paper›PMID 23832665›Full record

ArticleCancer research2013

Distinct FAK activities determine progenitor and mammary stem cell characteristics.

Ming Luo, Xiaofeng Zhao, Song Chen, Suling Liu, Max S Wicha, Jun-Lin Guan

Abstract readComparative Study
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-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

43 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  7. Review
  8. Review
  9. FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022
    Review
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  11. Review
  12. Article
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  14. Review
  15. FAK Promotes Early Osteoprogenitor Cell Proliferation by Enhancing mTORC1 Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  16. Review
  17. Article
  18. Article
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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 1 institution in 1 country.

Ming LuoDivisions of Molecular Medicine and Genetics and Hematology and Oncology, Department of Internal Medicine, Comprehensive Cancer Center, and Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Xiaofeng Zhao
Song Chen
Suling Liu
Max S Wicha
Jun-Lin Guan
University of Michigan–Ann Arbor · US

Funding

Genetic Analysis of FAK kinase and scaffold functions in breast cancerR01CA163493 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2012 to 2016
$1.6M
Molecular Analysis of Signal Transduction in Cancer Development and ProgressionR01CA150926 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2010 to 2014
$1.4M
NCI NIH HHS R01 CA150926NCI NIH HHS R01 CA163493
6 · The paper itself

Abstract

Mammary stem cells (MaSC) and progenitor cells are important for mammary gland development and maintenance and may give rise to mammary cancer stem cells (MaCSC). Yet, there remains limited understanding of how these cells contribute to tumorigenesis. Here, we show that conditional deletion of focal adhesion kinase (FAK) in embryonic mammary epithelial cells (MaEC) decreases luminal progenitors and basal MaSCs, reducing their colony-forming and regenerative potentials in a cell-autonomous manner. Loss of FAK kinase activity in MaECs specifically impaired luminal progenitor proliferation and alveologenesis, whereas a kinase-independent activity of FAK supported ductal invasion and basal MaSC activity. Deficiency in luminal progenitors suppressed tumorigenesis and MaCSC formation in a mouse model of breast cancer. In contrast with the general inhibitory effect of FAK attenuation, inhibitors of FAK kinase preferentially inhibited proliferation and tumorsphere formation of luminal progenitor-like, but not MaSC-like, human breast cancer cells. Our findings establish distinct kinase-dependent and -independent activities of FAK that differentially regulate luminal progenitors and basal MaSCs. We suggest that targeting these distinct functions may tailor therapeutic strategies to address breast cancer heterogeneity more effectively.

Indexed as

AnimalsApoptosisBlotting, WesternCarcinogenesisCell ProliferationFemaleFlow CytometryFluorescent Antibody TechniqueFocal Adhesion Protein-Tyrosine KinasesMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMutationNeoplasm InvasivenessNeoplastic Stem CellsPhosphorylationFocal Adhesion Protein-Tyrosine KinasesRNA, MessengerRNA, Small Interfering

Identifiers

PMID23832665
PMCPMC3766468
OpenAlexW2016512775

What OpenQuestion holds

Textmetadata
LicenceTDM
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.