ArticleOncoTargets and therapy2016
Histone deacetylase inhibitor sodium butyrate suppresses proliferation and promotes apoptosis in osteosarcoma cells by regulation of the MDM2-p53 signaling.
Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Sodium butyrate-induced autophagy in colorectal cancer unveils the Ca²⁺/CaMKKβ signaling pathway as a potential therapeutic target.Scientific reports · 2025Article
- Systemic strategies for osteosarcoma: advances and future directions.Discover oncology · 2025Review
- Combination of Selenite and Butyrate Enhances Efficacy Against Colon Cancer by Targeting ASCT2-Mediated Amino Acid Metabolism.Biological trace element research · 2024Article
- Multi-omic profiling reveals associations between the gut microbiome, host genome and transcriptome in patients with colorectal cancer.Journal of translational medicine · 2024Article
- Cisplatin and doxorubicin chemotherapy alters gut microbiota in a murine osteosarcoma model.Aging · 2024Article
- Comprehensive Analysis of Tumor Microenvironment Reveals Prognostic ceRNA Network Related to Immune Infiltration in Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Sodium Butyrate Induces Mitophagy and Apoptosis of Bovine Skeletal Muscle Satellite Cells through the Mammalian Target of Rapamycin Signaling Pathway.International journal of molecular sciences · 2023Article
- Butyrate inhibits the mitochondrial complex Ι to mediate mitochondria-dependent apoptosis of cervical cancer cells.BMC complementary medicine and therapies · 2023Article
- Osteosarcoma mechanobiology and therapeutic targets.British journal of pharmacology · 2022Review
- Article
- miR‑181b‑p53 negative feedback axis regulates osteosarcoma cell proliferation and invasion.International journal of molecular medicine · 2020Article
- Effects of Intestinal Microbial⁻Elaborated Butyrate on Oncogenic Signaling Pathways.Nutrients · 2019Review
- Protein profiling of osteosarcoma tissue and soft callus unveils activation of the unfolded protein response pathway.International journal of oncology · 2019Article
- MicroRNA-504 modulates osteosarcoma cell chemoresistance to cisplatin by targeting p53.Oncology letters · 2019Article
- Expression patterns of class I histone deacetylases in osteosarcoma: a novel prognostic marker with potential therapeutic implications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- Article
- The role and possible molecular mechanism of valproic acid in the growth of MCF-7 breast cancer cells.Croatian medical journal · 2017Article
- Therapeutic applications of histone deacetylase inhibitors in sarcoma.Cancer treatment reviews · 2017Review
- Methylation regulates HEY1 expression in glioblastoma.Oncotarget · 2017Article
- Resistance to cancer chemotherapeutic drugs is determined by pivotal microRNA regulators.American journal of cancer research · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors have been reported to induce tumor cell growth arrest, differentiation, and apoptosis. This study aimed to investigate the effects of one histone deacetylase inhibitor - sodium butyrate (SB) - on osteosarcoma (OS) cell proliferation and apoptosis and also the molecular mechanisms by which SB exerts regulatory effects on OS cells. U2OS and MG63 cells were treated with SB at various concentrations. Then, cell proliferation and apoptosis were determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide and flow cytometry assays, respectively; the expression of Ki67, Bax, Bcl-2, MDM2, and p53 proteins was determined by using Western blot assay. The results showed that SB suppressed proliferation in a concentration-dependent manner and promoted apoptosis of OS cells. In addition, SB enhanced p53 expression and decreased MDM2 expression, indicating that SB can regulate MDM2-p53 feedback loop. p53 inhibited proliferation and promoted apoptosis, whereas MDM2 promoted proliferation and suppressed apoptosis, which indicated that functional effect of SB on OS cell lines at least in part depended on the MDM2-p53 signaling. We also explored the effect of SB on OS cells in vivo and found that SB suppressed the growth of OS cells with no noticeable effect on activity and body weight of mice in vivo. These findings will offer new clues for OS development and progression and offer SB as a potent targeted agent for OS treatment.
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