Evidence map›Paper›PMID 25915847›Full record

ArticleOncogene2016

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression.

A Shvab, G Haase, A Ben-Shmuel, N Gavert, T Brabletz, S Dedhar, A Ben-Ze'ev

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 82 citations in OpenAlex.

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  13. Analysis ofInternational journal of ophthalmology · 2024
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  19. Fibroblastic SMOC2 Suppresses Mechanical Nociception by Inhibiting Coupled Activation of Primary Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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

7 authors at 3 institutions in 3 countries.

A ShvabDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
G HaaseDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
A Ben-ShmuelDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
N GavertDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-1639-4684
T BrabletzDepartment of Experimental Medicine 1, University of Erlangen-Nuernberg, Erlangen, Germany.
S DedharDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
A Ben-Ze'evDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · ILFriedrich-Alexander-Universität Erlangen-Nürnberg · DEOccupational Cancer Research Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overactivation of Wnt-β-catenin signaling, including β-catenin-TCF target gene expression, is a hallmark of colorectal cancer (CRC) development. We identified the immunoglobulin family of cell-adhesion receptors member L1 as a β-catenin-TCF target gene preferentially expressed at the invasive edge of human CRC tissue. L1 can confer enhanced motility and liver metastasis when expressed in CRC cells. This ability of L1-mediated metastasis is exerted by a mechanism involving ezrin and the activation of NF-κB target genes. In this study, we identified the secreted modular calcium-binding matricellular protein-2 (SMOC-2) as a gene activated by L1-ezrin-NF-κB signaling. SMOC-2 is also known as an intestinal stem cell signature gene in mice expressing Lgr5 in cells at the bottom of intestinal crypts. The induction of SMOC-2 expression in L1-expressing CRC cells was necessary for the increase in cell motility, proliferation under stress and liver metastasis conferred by L1. SMOC-2 expression induced a more mesenchymal like phenotype in CRC cells, a decrease in E-cadherin and an increase in Snail by signaling that involves integrin-linked kinase (ILK). SMOC-2 was localized at the bottom of normal human colonic crypts and at increased levels in CRC tissue with preferential expression in invasive areas of the tumor. We found an increase in Lgr5 levels in CRC cells overexpressing L1, p65 or SMOC-2, suggesting that L1-mediated CRC progression involves the acquisition of a stem cell-like phenotype, and that SMOC-2 elevation is necessary for L1-mediated induction of more aggressive/invasive CRC properties.

Indexed as

AnimalsCalcium-Binding ProteinsCell Growth ProcessesCell Line, TumorCell MovementColonic NeoplasmsDisease ProgressionHeterograftsHumansIntestinal MucosaIntestinesMiceMice, NudeNeoplasm MetastasisNeoplastic Stem CellsStem CellsCalcium-Binding ProteinsSMOC2 protein, human

Identifiers

PMID25915847
OpenAlexW1998507492

What OpenQuestion holds

Textmetadata
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.