{
  "abstract": "Hypoxia and epigenetic dysregulation are key contributors to breast cancer progression and therapeutic resistance. However, the interaction between histone deacetylase (HDAC) inhibition and hypoxia-associated signaling remains incompletely understood. This study therefore aimed to evaluate the combined effects of sodium butyrate (NaBu), an HDAC inhibitor, and cobalt chloride (CoCl ₂ ), a chemical hypoxia-mimetic agent, on the biological behavior of MCF-7 breast cancer cells. To do this, cells were treated with NaBu, CoCl ₂ , or their combination. Cell viability, proliferation, intracellular reactive oxygen species (ROS) generation, and cell-cycle distribution were assessed using MTT, cell counting, NBT, and flow cytometry, respectively. Quantitative real-time PCR was also performed to evaluate the expression of HDAC1 , HIF-1α , c-MET , and lncRNA-H19 . NaBu reduced cell viability and proliferation in a dose- and time-dependent manner, accompanied by increased ROS generation and HDAC1 downregulation. CoCl ₂ induced a hypoxia-mimetic response characterized by HIF-1α and lncRNA-H19 upregulation and G2/Marrest, whereas prolonged or higher-dose exposure promoted ROS accumulation and growth inhibition. Combined treatment further reduced cell viability and proliferation, enhanced ROS accumulation, and modulated hypoxia-related gene expression compared with either treatment alone. Although G2/M arrest was also observed following combined treatment, the cell-cycle profile largely resembled that induced by CoCl ₂ alone, suggesting that hypoxia-mimetic signaling predominantly drove this response. Overall, HDAC inhibition enhanced the cellular response to hypoxia-mimetic stress, highlighting the therapeutic potential of integrating epigenetic modulation with hypoxia-targeting strategies. Nevertheless, further mechanistic, drug-interaction, and in vivo studies are required to validate these findings.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "name": "Hadis Yari"
    },
    {
      "name": "Sajjad Sisakhtnezhad",
      "orcid": "0000-0001-7747-0324"
    },
    {
      "name": "Ali Bidmeshkipour"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/69kttc83608tr.bib",
  "cited_by": 0,
  "doi": "10.1038/s41598-026-73344-7",
  "fulltext_url": null,
  "id": "69kttc83608tr",
  "issns": [
    "2045-2322"
  ],
  "landing_url": "https://www.nature.com/articles/s41598-026-73344-7",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "1312|Histone Deacetylase Inhibitors Research"
    ]
  ],
  "openalex": "W7220833111",
  "pdf_url": "https://www.nature.com/articles/s41598-026-73344-7_reference.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-07",
  "publisher": "Springer Science and Business Media LLC",
  "ris": "https://research.draconitic.com/paper/69kttc83608tr.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:24Z",
      "native_id": "10.1038/s41598-026-73344-7",
      "source": "crossref",
      "url": "https://www.nature.com/articles/s41598-026-73344-7"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "openalex:1312|Histone Deacetylase Inhibitors Research",
      "subfield": "molecular-biology"
    }
  ],
  "title": "Sodium butyrate-mediated HDAC inhibition under hypoxic conditions modulates redox balance and tumor cell behavior in MCF-7 human breast cancer cells",
  "title_text": "Sodium butyrate-mediated HDAC inhibition under hypoxic conditions modulates redox balance and tumor cell behavior in MCF-7 human breast cancer cells",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:24Z",
  "url": "https://research.draconitic.com/paper/69kttc83608tr",
  "venue": "Scientific Reports",
  "versions": []
}