Evidence map›Paper›PMID 28079159›Full record

ArticleScientific reports2017

SOCS1 favors the epithelial-mesenchymal transition in melanoma, promotes tumor progression and prevents antitumor immunity by PD-L1 expression.

R Berzaghi, V S C Maia, F V Pereira, F M Melo, M S Guedes, C S T Origassa, J B Scutti, A L Matsuo, N O S Câmara, E G Rodrigues and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. SOCS1 Inhibits IL-6-Induced CD155 Overexpression in Lung Adenocarcinoma.International journal of molecular sciences · 2024
    Article
  6. Article
  7. A limitless Brazilian scientist: Professor Travassos and his contribution to cancer biology.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Review
  8. Article
  9. Article
  10. Review
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  14. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

R BerzaghiExperimental Oncology Unit, Department of Microbiology, Immunology and Parasitology, University of São Paulo, São Paulo, Brazil.
V S C MaiaRecepta Biopharma São Paulo, Brazil.
F V PereiraLaboratory of Cancer Immunobiology, University of São Paulo, São Paulo, Brazil.
F M MeloImmunology Department, Federal University of São Paulo, São Paulo, Brazil.
M S GuedesExperimental Oncology Unit, Department of Microbiology, Immunology and Parasitology, University of São Paulo, São Paulo, Brazil.
C S T OrigassaLaboratory of Cancer Immunobiology, University of São Paulo, São Paulo, Brazil.
J B ScuttiImmunotherapy Platform, Department of Immunology, MD Anderson Cancer Center, Houston Texas, USA.
A L MatsuoInterdepartmental Group of Health Economics (Grides), Federal University of São Paulo, SP, Brazil.
N O S CâmaraImmunology Department, Biomedical Sciences Institute IV, University of São Paulo, São Paulo, Brazil.
E G RodriguesLaboratory of Cancer Immunobiology, University of São Paulo, São Paulo, Brazil.
L R TravassosExperimental Oncology Unit, Department of Microbiology, Immunology and Parasitology, University of São Paulo, São Paulo, Brazil.
Universidade Federal de São Paulo · BRUniversidade de São Paulo · BRThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silencing of SOCS1 protein with shRNAi lentivirus (shR-SOCS1) led to partial reversion of the tumorigenic phenotype of B16F10-Nex2 melanoma cells. SOCS1 silencing inhibited cell migration and invasion as well as in vitro growth by cell cycle arrest at S phase with increased cell size and nuclei. Down-regulation of SOCS1 decreased the expression of epidermal growth factor receptor, Ins-Rα, and fibroblast growth factor receptors. The present work aimed at analyzing the SOCS1 cell signaling and expression of proteins relevant to tumor development. An RNA microarray analysis of B16F10-Nex2 melanoma cells with SOCS1 silenced by shRNAi-SOCS1 was undertaken in comparison with cells transduced with the empty vector. Among 609 differentially expressed genes, c-Kit, Met and EphA3 cytokine/tyrosine-kinase (TK) receptors were down regulated. A significant decrease in the expression of TK receptors, the phosphorylation of mediators of ERK1/2 and p38 pathways and STAT3 (S727) were observed. Subcutaneous immunization with shR-SOCS1-transduced viable tumor cells rendered protection against melanoma in a syngeneic model, with decreased expression of PD-L1 and of matrix metallo-proteinases (MMPs) and CD-10 in those cells. The present work shows the role of SOCS1 in murine melanoma development and the potential of SOCS1-silenced tumor cells in raising an effective anti-melanoma immune response.

Indexed as

Disease ProgressionEpithelial-Mesenchymal TransitionImmunityAnimalsB7-H1 AntigenBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsCD8-Positive T-LymphocytesCyclic AMP Response Element-Binding ProteinGene Expression Regulation, NeoplasticGene SilencingMelanoma, ExperimentalMelanoma-Specific AntigensMice, Inbred C57BLNF-kappa BProtective AgentsB7-H1 AntigenBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsCd274 protein, mouseCyclic AMP Response Element-Binding ProteinMelanoma-Specific AntigensNF-kappa BProtective AgentsReceptor Protein-Tyrosine KinasesSmad ProteinsSocs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinTranscription Factor AP-2Transforming Growth Factor beta

Identifiers

PMID28079159
PMCPMC5227698
OpenAlexW2579445581

What OpenQuestion holds

Textmetadata
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.