Evidence map›Paper›PMID 31278347›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

Search for novel STAT3-dependent genes reveals SERPINA3 as a new STAT3 target that regulates invasion of human melanoma cells.

Dorota W Kulesza, Kavita Ramji, Marta Maleszewska, Jakub Mieczkowski, Michal Dabrowski, Salem Chouaib, Bozena Kaminska

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In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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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 2 institutions in 3 countries.

Dorota W KuleszaLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland.
Kavita RamjiLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland.
Marta MaleszewskaLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland.
Jakub MieczkowskiLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland.
Michal DabrowskiLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland.
Salem ChouaibINSERM UMR1186, Integrative Tumor Immunology and Genetic Oncology, Institute Gustave Roussy, Viallejif, France.
Bozena KaminskaLaboratory of Molecular Neurobiology, Neurobiology Center, The Nencki Institute of Experimental Biology, Warsaw, Poland. b.kaminska@nencki.gov.pl.ORCID http://orcid.org/0000-0002-2642-4616
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in many cancers and promotes uncontrolled tumor growth and progression through multiple mechanisms. Compelling evidence shows tissue and cell-specific sets of STAT3 targets. Transcriptional targets of STAT3 in melanoma cells are largely unknown. Malignant melanoma is a deadly disease with highly aggressive and drug-resistant behavior. Less than 10% of patients with advanced melanomas reach the 5-year survival, partly due to the aggressive character of the tumor and ineffectiveness of current therapeutics for treating metastatic melanoma. STAT3 is constitutively activated in melanoma cells and plays important roles in its growth and angiogenesis in tumor xenograft studies. Moreover, highly metastatic melanoma cells have higher levels of active STAT3 than poorly metastatic ones. To identify genes that are driven by STAT3 in human melanoma cells, we performed JAK/STAT signaling specific and global gene expression profiling of human melanoma cells with silenced STAT3 expression. For selected genes, we performed computational identification of putative STAT3-binding sites and validated direct interactions STAT3 with defined promoters by using chromatin immunoprecipitation followed by qPCR. We found that STAT3 knockdown does not affect human melanoma cell viability, proliferation, or response to chemotherapeutics. We show that STAT3 regulates a discrete set of genes in melanoma cells, including SERPINA3, a novel STAT3 target gene, which is functionally involved in regulation of melanoma migration and invasion. Knockdown of STAT3 impaired cell migration and invasion, in part via regulation of its transcriptional target SERPINA3. Our results present novel targets and functions of STAT3 in melanoma cells.

Indexed as

Binding SitesCell Line, TumorCell MovementCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene Regulatory NetworksHumansMelanomaNeoplasm InvasivenessPhosphorylationPromoter Regions, GeneticSerpinsSignal TransductionSTAT3 Transcription FactorSERPINA3 protein, humanSerpinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID31278347
OpenAlexW2954464317

What OpenQuestion holds

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Registered trials

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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.