Evidence map›Paper›PMID 31865754›Full record

ArticleJournal of enzyme inhibition and medicinal chemistry2020

A potentiated cooperation of carbonic anhydrase IX and histone deacetylase inhibitors against cancer.

Jessica Ruzzolini, Anna Laurenzana, Elena Andreucci, Silvia Peppicelli, Francesca Bianchini, Fabrizio Carta, Claudiu T Supuran, Maria Novella Romanelli, Chiara Nediani, Lido Calorini

Abstract read
In one paragraph

Article in Journal of enzyme inhibition and medicinal chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
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  4. Review
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  8. Review
  9. Hybrid inhibitors of DNA and HDACs remarkably enhance cytotoxicity in leukaemia cells.Journal of enzyme inhibition and medicinal chemistry · 2020
    Article
  10. Review
  11. Article
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

10 authors.

Jessica RuzzoliniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Anna LaurenzanaDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Elena AndreucciDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Silvia PeppicelliDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Francesca BianchiniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Fabrizio CartaDepartment of NEUROFARBA, University of Florence, Florence, Italy.
Claudiu T SupuranDepartment of NEUROFARBA, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0003-4262-0323
Maria Novella RomanelliDepartment of NEUROFARBA, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0002-5685-3403
Chiara NedianiDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Lido CaloriniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The emergence of tumour recurrence and resistance limits the survival rate for most tumour-bearing patients. Only, combination therapies targeting pathways involved in the induction and in the maintenance of cancer growth and progression might potentially result in an enhanced therapeutic efficacy. Herein, we provided a prospective combination treatment that includes suberoylanilide hydroxamic acid (SAHA), a well-known inhibitor of histone deacetylases (HDACs), and SLC-0111, a novel inhibitor of carbonic anhydrase (CA) IX. We proved that HDAC inhibition with SAHA in combination with SLC-0111 affects cell viability and colony forming capability to greater extent than either treatment alone of breast, colorectal and melanoma cancer cells. At the molecular level, this therapeutic regimen resulted in a synergistically increase of histone H4 and p53 acetylation in all tested cell lines. Overall, our findings showed that SAHA and SLC-0111 can be regarded as very attractive combination providing a potential therapeutic strategy against different cancer models.

Indexed as

Antigens, NeoplasmAntineoplastic AgentsCarbonic Anhydrase InhibitorsCarbonic Anhydrase IXCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorHistone Deacetylase InhibitorsHistone DeacetylasesHumansMolecular StructurePhenylurea CompoundsStructure-Activity RelationshipSulfonamidesTumor Cells, CulturedAntigens, NeoplasmAntineoplastic AgentsCA9 protein, humanCarbonic Anhydrase InhibitorsCarbonic Anhydrase IXHistone Deacetylase InhibitorsHistone DeacetylasesPhenylurea CompoundsSLC-0111SulfonamidesCarbonic anhydrase IXcombined therapyhistone acetylationSLC-0111;SAHA

Identifiers

PMID31865754
PMCPMC6968260

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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.