Evidence map›Paper›PMID 28929255›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2017

Carbonic anhydrase IX inhibition affects viability of cancer cells adapted to extracellular acidosis.

Elena Andreucci, Silvia Peppicelli, Fabrizio Carta, Giulia Brisotto, Eva Biscontin, Jessica Ruzzolini, Francesca Bianchini, Alessio Biagioni, Claudiu T Supuran, Lido Calorini

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 93 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

10 authors at 4 institutions in 1 country.

Elena AndreucciDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Silvia PeppicelliDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Fabrizio CartaDepartment of NEUROFARBA, University of Florence, Florence, Italy.
Giulia BrisottoDISCOG, University of Padova, Padova, Italy.
Eva BiscontinImmunopathology and Cancer Biomarkers, Traslational Research Department, IRCCS, C.R.O. National Cancer Institute, Aviano, Pordenone, Italy.
Jessica RuzzoliniDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Francesca BianchiniDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy.
Alessio BiagioniDepartment of Surgery and Translational Medicine, University of Florence, Florence, Italy.
Claudiu T SupuranDepartment of NEUROFARBA, University of Florence, Florence, Italy.
Lido CaloriniDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy. lido.calorini@unifi.it.
University of Florence · ITTumour Institute of Tuscany · ITCentro di Riferimento Oncologico · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among the players of the adaptive response of cancer cells able to promote a resistant and aggressive phenotype, carbonic anhydrase IX (CAIX) recently has emerged as one of the most relevant drug targets. Indeed, CAIX targeting has received a lot of interest, and selective inhibitors are currently under clinical trials. Hypoxia has been identified as the master inductor of CAIX, but, to date, very few is known about the influence that another important characteristic of tumor microenvironment, i.e., extracellular acidosis, exerts on CAIX expression and activity. In the last decades, acidic microenvironment has been associated with aggressive tumor phenotype endowed with epithelial-to-mesenchymal transition (EMT) profile, high invasive and migratory ability, apoptosis, and drug resistance. We demonstrated that melanoma, breast, and colorectal cancer cells transiently and chronically exposed to acidified medium (pH 6.7 ± 0.1) showed a significantly increased CAIX expression compared to those grown in standard conditions (pH 7.4 ± 0.1). Moreover, we observed that the CAIX inhibitor FC16-670A (also named SLC-0111, which just successfully ended phase I clinical trials) not only prevents such increased expression under acidosis but also promotes apoptotic and necrotic programs only in acidified cancer cells. Thus, CAIX could represent a selective target of acidic cancer cells and FC16-670A inhibitor as a useful tool to affect this aggressive subpopulation characterized by conventional therapy escape. KEY MESSAGES: Cancer cells overexpress CAIX under transient and chronic extracellular acidosis. Acidosis-induced CAIX overexpression is NF-κB mediated and HIF-1α independent. FC16-670A prevents CAIX overexpression and induces acidified cancer cell death.

Indexed as

AcidosisAntigens, NeoplasmCarbonic Anhydrase InhibitorsCarbonic Anhydrase IXCell DeathCell Line, TumorCell ProliferationCell SurvivalExtracellular SpaceHumansPhenylurea CompoundsSulfonamidesAntigens, NeoplasmCA9 protein, humanCarbonic Anhydrase InhibitorsCarbonic Anhydrase IXPhenylurea CompoundsSLC-0111SulfonamidesAcidosis of tumor microenvironmentApoptosisCarbonic anhydrase IX (CAIX)FC16-670A CAIX inhibitor

Identifiers

PMID28929255
OpenAlexW2755386227

What OpenQuestion holds

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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.