Evidence map›Paper›PMID 33446633›Full record

ArticleOncogenesis2021

Prolactin receptor-driven combined luminal and epithelial differentiation in breast cancer restricts plasticity, stemness, tumorigenesis and metastasis.

Anwar Shams, Najat Binothman, Julien Boudreault, Ni Wang, Fuad Shams, Dana Hamam, Jun Tian, Alaa Moamer, Meiou Dai, Jean-Jacques Lebrun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  6. Article
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  8. Article
  9. Article
  10. Article
  11. Emerging Roles of RNF168 in Tumor Progression.Molecules (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Review
  14. Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Review
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

11 authors at 4 institutions in 2 countries.

Anwar ShamsDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Najat BinothmanDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Julien BoudreaultDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Ni WangDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Fuad ShamsDepartment of Pathology and Laboratory Medicine, King Abdulaziz Hospital, Mecca, Saudi Arabia.
Dana HamamDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Jun TianDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Alaa MoamerDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Meiou DaiDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Jean-Jacques LebrunDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Suhad AliDepartment of Medicine, Cancer Research Program, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada. suhad.ali@mcgill.ca.ORCID http://orcid.org/0000-0002-9027-6232
McGill University Health Centre · CAKing Abdulaziz Hospital · SAKing Abdulaziz University · SATaif University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dedifferentiation increased cellular plasticity and stemness are established derivers of tumor heterogeneity, metastasis and therapeutic failure resulting in incurable cancers. Therefore, it is essential to decipher pro/forward-differentiation mechanisms in cancer that may serve as therapeutic targets. We found that interfering with expression of the receptor for the lactogenic hormone prolactin (PRLR) in breast cancer cells representative of the luminal and epithelial breast cancer subtypes (hormone receptor positive (HR+) and HER2-enriched (HER2-E) resulted in loss of their differentiation state, enriched for stem-like cell subpopulations, and increased their tumorigenic capacity in a subtype-specific manner. Loss of PRLR expression in HR+ breast cancer cells caused their dedifferentiation generating a mesenchymal-basal-like phenotype enriched in CD44+ breast cancer stem-like cells (BCSCs) showing high tumorigenic and metastatic capacities and resistance to anti-hormonal therapy. Whereas loss of PRLR expression in HER2-E breast cancer cells resulted in loss of their luminal differentiation yet enriched for epithelial ALDH+ BCSC population showing elevated HER2-driven tumorigenic, multi-organ metastatic spread, and resistance to anti-HER2 therapy. Collectively, this study defines PRLR as a driver of precise luminal and epithelial differentiation limiting cellular plasticity, stemness, and tumorigenesis and emphasizing the function of pro/forward-differentiation pathways as a foundation for the discovery of anti-cancer therapeutic targets.

Identifiers

PMID33446633
PMCPMC7809050
OpenAlexW3121035950

What OpenQuestion holds

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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.