Evidence map›Paper›PMID 22751124›Full record

ArticleOncogene2013

p21CIP1 mediates reciprocal switching between proliferation and invasion during metastasis.

X Qian, J Hulit, K Suyama, E A Eugenin, T J Belbin, O Loudig, T Smirnova, Z N Zhou, J Segall, J Locker and 3 more

Abstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  12. Actin dynamics during tumor cell dissemination.International review of cell and molecular biology · 2021
    Review
  13. Aryl Hydrocarbon Receptor Connects Inflammation to Breast Cancer.International journal of molecular sciences · 2020
    Review
  14. Review
  15. Article
  16. Review
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  19. 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

13 authors at 4 institutions in 1 country.

X Qian *Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
J Hulit *Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
K SuyamaDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
E A EugeninDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
T J BelbinDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
O LoudigDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
T SmirnovaDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
Z N ZhouDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
J SegallDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
J LockerDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
G R PhillipsDepartment of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.
L NortonDepartment of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
R B HazanDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
Albert Einstein College of Medicine · USIcahn School of Medicine at Mount Sinai · USMemorial Sloan Kettering Cancer Center · USYeshiva University · US

Funding

Astrocyte connexin43 containing channels amplify CNS dysfunction in NeuroAIDSR01MH096625 · NIMH · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI EUGENIN, ELISEO A · 2012 to 2020
$4.5M
EMT, Extravasation and metastasis by N-Cadherin signalingR01CA135061 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HAZAN, RACHEL B · 2009 to 2013
$1.7M
The role of gap junction channels in NeuroAIDSK01MH076679 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI EUGENIN, ELISEO A · 2006 to 2010
$646k
NCI NIH HHS 1R01 CA135061-01A1NCI NIH HHS R01 CA135061NIMH NIH HHS K01 MH076679NIMH NIH HHS R01 MH096625
6 · The paper itself

Abstract

Cell proliferation and invasion are critical for malignant progression, yet how these processes relate to each other and whether they regulate one another during metastasis is unknown. We show that invasiveness of breast cancer cells is associated with growth arrest due to p21CIP1 upregulation. Knockdown of p21CIP1 increases cell proliferation and suppresses invasion. Since p21CIP1 acts to inhibit cyclin E during cell-cycle progression, we demonstrated that a constitutively active form of cyclin E had similar effects to p21CIP1 inhibition resulting in enhanced cell growth and suppressed invasiveness. We tested these findings in vivo in the Polyoma middle T mammary tumor model in which p21CIP1 was deleted. p21CIP1 knockout mice exhibited dramatic suppression of metastasis, independent of tumor growth, which was rescued by p21CIP1. Metastasis suppression by p21CIP1 ablation was associated with striking cytoskeletal reorganization leading to a non-invasive and highly proliferative state. Thus, p21CIP1 regulates metastasis by mediating reciprocal switching between invasion and proliferation.

Indexed as

AnimalsBreast NeoplasmsCell MovementCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin ECytoskeletonFemaleG1 Phase Cell Cycle CheckpointsGene Knockout TechniquesHumansMammary Neoplasms, ExperimentalMiceMice, TransgenicNeoplasm MetastasisCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin E

Identifiers

PMID22751124
PMCPMC4350674
OpenAlexW2008552477

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.