Evidence map›Paper›PMID 30967481›Full record

ArticleMolecular cancer research : MCR2019

p21CIP1 Promotes Mammary Cancer-Initiating Cells via Activation of Wnt/TCF1/CyclinD1 Signaling.

Outhiriaradjou Benard, Xia Qian, Huizhi Liang, Zuen Ren, Kimita Suyama, Larry Norton, Rachel B Hazan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023
    Review
  6. Article
  7. Article
  8. Article
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  10. Review
  11. 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

7 authors at 2 institutions in 1 country.

Outhiriaradjou Benard *Department of Pathology, Albert Einstein College of Medicine, Bronx, New York.
Xia Qian *Department of Pathology, Albert Einstein College of Medicine, Bronx, New York.
Huizhi LiangDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York.
Zuen RenDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York.ORCID 0000-0001-5951-1292
Kimita SuyamaDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York.
Larry NortonDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
Rachel B HazanDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York. Rachel.hazan@einstein.yu.edu.
Albert Einstein College of Medicine · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Mechanisms of N-Cadherin Mediated Breast CA MetastasisR01CA090872 · NCI · YESHIVA UNIVERSITY · PI HAZAN, RACHEL B · 2002 to 2005
$1.2M
NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA013330NCI NIH HHS R01 CA090872
6 · The paper itself

Abstract

Cancer stem cells (CSC) generate and sustain tumors due to tumor-initiating potential, resulting in recurrence or metastasis. We showed that knockout of the cell-cycle inhibitor, p21CIP1, in the PyMT mammary tumor model inhibits metastasis; however the mechanism remained unknown. Here, we show a pivotal role for p21 in potentiating a cancer stem-like phenotype. p21 knockout in PyMT mammary tumor cells caused dramatic suppression of CSC properties involving tumorsphere formation, ALDH1 activity, and tumor-initiating potential, which were in turn rescued by p21 overexpression into PyMT/p21 knockout cells. Interestingly, p21 knockout dramatically suppresses Wnt/β-catenin signaling activity, leading to striking inhibition of LEF1 and TCF1 expression. TCF1 knockdown in PyMT cells suppressed tumorsphere formation due to Cyclin D1 attenuation. These data demonstrate that p21 promotes a CSC-like phenotype via activation of Wnt/TCF1/Cyclin D1 signaling. IMPLICATIONS: p21 is a strong promoter of mammary CSCs.

Indexed as

Aldehyde Dehydrogenase 1 FamilyAnimalsBreastBreast NeoplasmsCell Line, TumorCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p21FemaleGene Knockout TechniquesHepatocyte Nuclear Factor 1-alphaHumansLymphoid Enhancer-Binding Factor 1Mammary Neoplasms, AnimalNeoplasm Recurrence, LocalNeoplastic Stem CellsAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, mouseCdkn1a protein, mouseCyclin D1Cyclin-Dependent Kinase Inhibitor p21Hepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Retinal Dehydrogenase

Identifiers

PMID30967481
PMCPMC7793565
OpenAlexW2935776191

What OpenQuestion holds

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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.