Evidence map›Paper›PMID 28823832›Full record

ArticleExperimental cell research2017

The adaptor SASH1 acts through NOTCH1 and its inhibitor DLK1 in a 3D model of lumenogenesis involving CEACAM1.

Kandis Stubblefield, Jennifer Chean, Tung Nguyen, Charng-Jui Chen, John E Shively

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
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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

5 authors at 2 institutions in 1 country.

Kandis StubblefieldIrell and Manella Graduate School of Biological Sciences of City of Hope, 1450 East Duarte Rd, Duarte CA 91010, United States.
Jennifer CheanDepartment of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E Duarte, Rd, Duarte CA 91010, United States.
Tung NguyenDepartment of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E Duarte, Rd, Duarte CA 91010, United States.
Charng-Jui ChenDepartment of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E Duarte, Rd, Duarte CA 91010, United States.
John E ShivelyDepartment of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E Duarte, Rd, Duarte CA 91010, United States. Electronic address: jshively@coh.org.
City of Hope · USBeckman Research Institute

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI XIWEI WU · 1985 to 2026
$86.3M
Role of CEACAM1 in Epithelial Cell PolarizationR01CA084202 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI SHIVELY, JOHN ERNEST · 2000 to 2010
$4.1M
NCI NIH HHS P30 CA033572NCI NIH HHS R01 CA084202
6 · The paper itself

Abstract

CEACAM1 transfection into breast cancer cells restores lumen formation in a 3D culture model. Among the top up-regulated genes that were associated with restoration of lumen formation, the adaptor protein SASH1 was identified. Furthermore, SASH1 was shown to be critical for lumen formation by RNAi inhibition. Upon analyzing the gene array from CEACAM1/MCF7 cells treated with SASH1 RNAi, DLK1, an inhibitor of NOTCH1 signaling, was found to be down-regulated to the same extent as SASH1. Subsequent treatment of CEACAM1/MCF7 cells with RNAi to DLK1 also inhibited lumen formation, supporting its association with SASH1. In agreement with the role of DLK1 as a NOTCH1 inhibitor, NOTCH1, as well as its regulated genes HES1 and HEY1, were down-regulated in CEACAM1/MCF7 cells by the action of DLK1 RNAi, and up-regulated by SASH1 RNAi. When CEACAM1/MCF7 cells were treated with a γ-secretase inhibitor known to inhibit NOTCH signaling, lumen formation was inhibited. We conclude that restoration of lumen formation by CEACAM1 regulates the NOTCH1 signaling pathway via the adaptor protein SASH1 and the NOTCH1 inhibitor DLK1. These data suggest that the putative involvement of NOTCH1 as a tumor-promoting gene in breast cancer may depend on its lack of regulation in cancer, whereas its involvement in normal lumen formation requires activation of its expression, and subsequently, inhibition of its signaling.

Indexed as

Amyloid Precursor Protein SecretasesAntigens, CDBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCell Adhesion MoleculesCell Culture TechniquesCell Cycle ProteinsFemaleGene Expression RegulationHumansIntercellular Signaling Peptides and ProteinsMCF-7 CellsMembrane ProteinsProtein BindingReceptor, Notch1RNA, Small InterferingAmyloid Precursor Protein SecretasesAntigens, CDBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCD66 antigensCell Adhesion MoleculesCell Cycle ProteinsDLK1 protein, humanHES1 protein, humanHEY1 protein, humanIntercellular Signaling Peptides and ProteinsMembrane ProteinsNOTCH1 protein, humanReceptor, Notch1RNA, Small InterferingSASH1 protein, humanTranscription Factor HES-1Tumor Suppressor ProteinsBreast cancerCEACAM1DLK1LumeogenesisNOTCH1SASH1

Identifiers

PMID28823832
PMCPMC8994489
OpenAlexW2747045788

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.