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caix inhibitor fc16-670a fc16-670a inhibitor month download article/chapter metalloprotease-dependent process regulated hypoxia-inducible factors 1alpha acidosis-induced caix overexpression nf-κb-dependent mechanisms istituto toscano tumori hypoxia-induced catalytic component carbonic anhydrase inhibition molecular medicine aims carbonic anhydrase ix alessio biagioni nf-κb mediated full article pdf molecular oncology unit aberrant focal adhesion privacy choices/manage cookies traslational research department acidic melanoma cells human melanoma cells hypoxia-inducible expression hypoxia induced genes acidic cancer cells chronic extracellular acidosis acidified cancer cells tumour hypoxia induces human glioblastoma cells human osteosarcoma cells author information authors cancer cells adapted hypoxia induced expression breast tumor growth dormant tumor cells european economic area relevant drug targets successfully ended phase aggressive subpopulation characterized related subjects metabolic pathway adaptation show antimetastatic activity auf dem keller van kuijk sj athymic nude mice continuous changing behavior aerobic glycolysis back carbonic anhydrases national cancer institute dual targeting drugs manipulating tumor acidification

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         headline:Carbonic anhydrase IX inhibition affects viability of cancer cells adapted to extracellular acidosis
         description: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.
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      headline:Carbonic anhydrase IX inhibition affects viability of cancer cells adapted to extracellular acidosis
      description: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.
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      name:Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, University of Florence, Florence, Italy
      name:Istituto Toscano Tumori (ITT), Florence, Italy
      name:Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, University of Florence, Florence, Italy
      name:Istituto Toscano Tumori (ITT), Florence, Italy
      name:Department of NEUROFARBA, University of Florence, Florence, Italy
      name:DISCOG, University of Padova, Padova, Italy
      name:Immunology and Molecular Oncology Unit, IOV-IRCCS, Padova, Italy
      name:Immunopathology and Cancer Biomarkers, Traslational Research Department, IRCCS, C.R.O. National Cancer Institute, Pordenone, Italy
      name:Immunopathology and Cancer Biomarkers, Traslational Research Department, IRCCS, C.R.O. National Cancer Institute, Pordenone, Italy
      name:Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, University of Florence, Florence, Italy
      name:Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, University of Florence, Florence, Italy
      name:Istituto Toscano Tumori (ITT), Florence, Italy
      name:Department of Surgery and Translational Medicine, University of Florence, Florence, Italy
      name:Department of NEUROFARBA, University of Florence, Florence, Italy
      name:Department of Clinical and Experimental Biomedical Sciences “Mario Serio”, University of Florence, Florence, Italy
      name:Istituto Toscano Tumori (ITT), Florence, Italy
      name:Excellence Centre for Research, Transfer and High Education DENOTHE, Florence, Italy
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