Evidence map›Paper›PMID 25686823›Full record

ArticleOncotarget2015

SNAI2/Slug gene is silenced in prostate cancer and regulates neuroendocrine differentiation, metastasis-suppressor and pluripotency gene expression.

Silvia Esposito, Marco V Russo, Irma Airoldi, Maria Grazia Tupone, Carlo Sorrentino, Giulia Barbarito, Serena Di Meo, Emma Di Carlo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-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

36 citing papers in PubMed, 47 citations in OpenAlex.

  1. Loss ofJCO precision oncology · 2021
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  7. Targeting Key Players of Neuroendocrine Differentiation in Prostate Cancer.International journal of molecular sciences · 2023
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  9. Article
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  11. 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

8 authors at 2 institutions in 1 country.

Silvia EspositoDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
Marco V RussoDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
Irma AiroldiLaboratory of Oncology, Istituto Giannina Gaslini, Genova, Italy.
Maria Grazia TuponeDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
Carlo SorrentinoDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
Giulia BarbaritoLaboratory of Oncology, Istituto Giannina Gaslini, Genova, Italy.
Serena Di MeoDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
Emma Di CarloDepartment of Medicine and Sciences of Aging, Section of Anatomic Pathology and Molecular Medicine, "G. d'Annunzio" University, Chieti, Italy.
University of Chieti-Pescara · ITIstituto Giannina Gaslini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate Cancer (PCa)-related deaths are mostly due to metastasization of poorly differentiated adenocarcinomas often endowed with neuroendocrine differentiation (NED) areas.The SNAI2/Slug gene is a major regulator of cell migration and tumor metastasization. We here assessed its biological significance in NED, and metastatic potential of PCa.SNAI2 expression was down-regulated in most PCa epithelia, in association with gene promoter methylation, except for cell clusters forming: a. the expansion/invasion front of high-grade PCa, b. NED areas, or c. lymph node metastasis.Knockdown of SNAI2 in PC3 cells down-regulated the expression of neural-tissue-associated adhesion molecules, Neural-Cadherin, Neural-Cadherin-2, Neuronal-Cell-Adhesion-Molecule, and of the NED marker Neuron-Specific Enolase, whereas it abolished Chromogranin-A expression. The metastasis-suppressor genes, Nm23-H1 and KISS1, were up-regulated, while the pluripotency genes SOX2, NOTCH1, CD44v6, WWTR1/TAZ and YAP1 were dramatically down-regulated. Over-expression of SNAI2 in DU145 cells substantiated its ability to regulate metastasis-suppressor, NED and pluripotency genes. In PCa and lymph node metastasis, expression of SOX2 and NOTCH1 was highly related to that of SNAI2.In conclusion, I. SNAI2 silencing in PCa may turn-off the expression of NED markers and pluripotency genes, while turning-on that of specific metastasis-suppressors, II. SNAI2 expression in selected PCa cells, by regulating their self-renewal, NED and metastatic potential, endows them with highly malignant properties. SNAI2 may thus constitute a key target for modern approaches to PCa progression.

Indexed as

Cell DifferentiationAdenocarcinomaAgedBlotting, WesternCell Line, TumorDNA MethylationDown-RegulationGene Expression Regulation, NeoplasticGene SilencingHumansImmunohistochemistryLaser Capture MicrodissectionMaleMiddle AgedNeoplasm MetastasisProstatic NeoplasmsSNAI1 protein, humanSNAI2 protein, humanSnail Family Transcription FactorsTranscription Factorslaser capture microdissectionneuroendocrine differentiationprostate cancerSNAI2/Slug

Identifiers

PMID25686823
PMCPMC4627296
OpenAlexW1610761134

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.