ArticleBMC cancer2017
Acetazolamide potentiates the anti-tumor potential of HDACi, MS-275, in neuroblastoma.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Combination therapy in combating cancer.Oncotarget · 2017Pooled it
- Cordycepin suppresses growth and virulence ofVirulence · 2026Article
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Carbonic anhydrases contribute to mitochondrial function, conidial development, and pathogenicity ofApplied and environmental microbiology · 2026Article
- Discovery of First-in-Class Carbonic Anhydrase/Histone Deacetylase Dual Inhibitors with Antiproliferative Activity in Cancer Cells.Journal of medicinal chemistry · 2025Article
- 4-Methylumbelliferone Modulates CAIX to Mitigate Hypoxia-Driven Dysregulation and Enhance PD-1 Immunotherapy in Lung Cancer.International journal of molecular sciences · 2025Article
- MS275 Inhibits Neuroblastoma Cell Growth by Mediating H3K27ac/PROX1 Axis In Silico and In Vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- LncRNA ZNF674-AS1 drives cell growth and inhibits cisplatin-induced pyroptosis via up-regulating CA9 in neuroblastoma.Cell death & disease · 2024Article
- GSE1 links the HDAC1/CoREST co-repressor complex to DNA damage.Nucleic acids research · 2023Article
- Chloroxylon swietenia (Roxb.) DC induces cell death and apoptosis by down-regulating the NF-κB pathway in MCF-7 breast cancer cells: In vitro and in vivo investigations.Cancer reports (Hoboken, N.J.) · 2022Article
- Glioblastoma: Current Status, Emerging Targets, and Recent Advances.Journal of medicinal chemistry · 2022Review
- Effects of acetazolamide on linear growth in children with pseudotumor cerebri syndrome.Frontiers in ophthalmology · 2022Article
- Carbonic Anhydrase IX Inhibitors as Candidates for Combination Therapy of Solid Tumors.International journal of molecular sciences · 2021Review
- Article
- Efficacy of a Three Drug-Based Therapy for Neuroblastoma in Mice.International journal of molecular sciences · 2021Article
- A potentiated cooperation of carbonic anhydrase IX and histone deacetylase inhibitors against cancer.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Towards an Integral Therapeutic Protocol for Breast Cancer Based upon the New HInternational journal of molecular sciences · 2020Review
- Review
- Histone Deacetylases and Histone Deacetylase Inhibitors in Neuroblastoma.Frontiers in cell and developmental biology · 2020Review
- Human bronchial carcinoid tumor initiating cells are targeted by the combination of acetazolamide and sulforaphane.BMC cancer · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroblastoma (NB), a tumor of the primitive neural crest, despite aggressive treatment portends a poor long-term survival for patients with advanced high stage NB. New treatment strategies are required.
methodsWe investigated coordinated targeting of essential homeostatic regulatory factors involved in cancer progression, histone deacetylases (HDACs) and carbonic anhydrases (CAs).
resultsWe evaluated the antitumor potential of the HDAC inhibitor (HDACi), pyridylmethyl-N-{4-[(2-aminophenyl)-carbamoyl]-benzyl}-carbamate (MS-275) in combination with a pan CA inhibitor, acetazolamide (AZ) on NB SH-SY5Y, SK-N-SH and SK-N-BE(2) cells. The key observation was that the combination AZ + MS-275 significantly inhibited growth, induced cell cycle arrest and apoptosis, and reduced migration capacity of NB cell line SH-SY5Y. In addition, this combination significantly inhibited tumor growth in vivo, in a pre-clinical xenograft model. Evidence was obtained for a marked reduction in tumorigenicity and in the expression of mitotic, proliferative, HIF-1α and CAIX. NB xenografts of SH-SY5Y showed a significant increase in apoptosis.
conclusionMS-275 alone at nanomolar concentrations significantly reduced the putative cancer stem cell (CSC) fraction of NB cell lines, SH-SY5Y and SK-N-BE(2), in reference to NT2/D1, a teratocarcinoma cell line, exhibiting a strong stem cell like phenotype in vitro. Whereas stemness genes (OCT4, SOX2 and Nanog) were found to be significantly downregulated after MS-275 treatment, this was further enhanced by AZ co-treatment. The significant reduction in initial tumorigenicity and subsequent abrogation upon serial xenografting suggests potential elimination of the NB CSC fraction. The significant potentiation of MS-275 by AZ is a promising therapeutic approach and one amenable for administration to patients given their current clinical utility.
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