Evidence map›Paper›PMID 31412593›Full record

ArticleBiomolecules2019

The Natural-Based Antitumor Compound T21 Decreases Survivin Levels through Potent STAT3 Inhibition in Lung Cancer Models.

David Martínez-García, Marta Pérez-Hernández, Luís Korrodi-Gregório, Roberto Quesada, Ricard Ramos, Núria Baixeras, Ricardo Pérez-Tomás, Vanessa Soto-Cerrato

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-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

14 citing papers in PubMed, 31 citations in OpenAlex.

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  8. Molecules (Basel, Switzerland) · 2021
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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 4 institutions in 1 country.

David Martínez-GarcíaDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, 08905 Barcelona, Spain.ORCID 0000-0001-7731-2107
Marta Pérez-HernándezDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, 08905 Barcelona, Spain.ORCID 0000-0003-1331-5493
Luís Korrodi-GregórioDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, 08905 Barcelona, Spain.
Roberto QuesadaDepartment of Chemistry, Universidad de Burgos, 09001 Burgos, Spain.ORCID 0000-0003-2764-7157
Ricard RamosDepartment of Thoracic Surgery and University of Barcelona, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, 08907 Barcelona, Spain.
Núria BaixerasDepartment of Pathology, Hospital Universitari de Bellvitge-IDIBELL, L'Hospitalet de Llobregat, 08907 Barcelona, Spain.
Ricardo Pérez-TomásDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, 08905 Barcelona, Spain.
Vanessa Soto-CerratoDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine and Health Sciences, Universitat de Barcelona, 08905 Barcelona, Spain. vsoto@ub.edu.ORCID 0000-0001-5835-3595
Institut d'Investigació Biomédica de Bellvitge · ESBellvitge University Hospital · ESUniversidad de Burgos · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide; hence novel treatments for this malignancy are eagerly needed. Since natural-based compounds represent a rich source of novel chemical entities in drug discovery, we have focused our attention on tambjamines, natural compounds isolated from marine invertebrates that have shown diverse pharmacological activities. Based on these structures, we have recently identified the novel indole-based tambjamine analog 21 (T21) as a promising antitumor agent, which modulates the expression of apoptotic proteins such as survivin. This antiapoptotic protein plays an important role in carcinogenesis and chemoresistance. In this work, we have elucidated the molecular mechanism by which the anticancer compound T21 exerts survivin inhibition and have validated this protein as a therapeutic target in different lung cancer models. T21 was able to reduce survivin protein levels in vitro by repressing its gene expression through the blockade of Janus kinase/Signal Transducer and Activator of Transcription-3 (JAK/STAT3)/survivin signaling pathway. Interestingly, this occurred even when the pathway was overstimulated with its ligand interleukin 6 (IL-6), which is frequently overexpressed in lung cancer patients who show poor clinical outcomes. Altogether, these results show T21 as a potent anticancer compound that effectively decreases survivin levels through STAT3 inhibition in lung cancer, appearing as a promising therapeutic drug for cancer treatment.

Indexed as

Antineoplastic AgentsBiological ProductsCarcinoma, Non-Small-Cell LungCell ProliferationCells, CulturedCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorHIV Envelope Protein gp41HumansLung NeoplasmsMolecular StructurePeptide FragmentsSTAT3 Transcription FactorStructure-Activity RelationshipSurvivinAntineoplastic AgentsBiological ProductsBIRC5 protein, humanHIV Envelope Protein gp41Peptide Fragmentspeptide T21STAT3 protein, humanSTAT3 Transcription FactorSurvivinanticancer therapyapoptosislung cancernatural-based compoundSTAT3survivin

Identifiers

PMID31412593
PMCPMC6724027
OpenAlexW2967533218

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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.