The Effect of Sodium Butyrate on Radiosensitivity in Glioblastoma Cell

Çakır, Tahir; Güven, Mustafa; Taşpınar, Mehmet; Denizler, Farika Nur; Kartal, Bahar

doi:10.5505/vtd.2019.24434

Cited by 1 publication

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“…Sodium butyrate (SB), an HDACi derived from a fatty acid, has gained attention due to its ability to inhibit class I and IIa HDACs [ 6 , 7 ]. Preclinical investigations have established the anti-neoplastic effects of sodium butyrate, both as a monotherapy and in combination with other chemotherapeutic agents, across various cancer types [ 8 – 12 ]. While the blood–brain barrier (BBB) represents a critical impediment to achieving effective treatments for GB [ 4 ], SB effectively overcomes this hurdle by exhibiting a remarkable ability to readily cross the BBB [ 13 ].…”

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confidence: 99%

Exploring the combined anti-cancer effects of sodium butyrate and celastrol in glioblastoma cell lines: a novel therapeutic approach

Kartal,

Denizler-Ebiri,

Güven

et al. 2024

Med Oncol

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Glioblastoma, a highly aggressive and lethal brain cancer, lacks effective treatment options and has a poor prognosis. In our study, we explored the potential anti-cancer effects of sodium butyrate (SB) and celastrol (CEL) in two glioblastoma cell lines. SB, a histone deacetylase inhibitor, and CEL, derived from the tripterygium wilfordii plant, act as mTOR and proteasome inhibitors. Both can cross the blood–brain barrier, and they exhibit chemo- and radiosensitive properties in various cancer models. GB cell lines LN-405 and T98G were treated with SB and CEL. Cell viability was assessed by MTT assay and IC50 values were obtained. Gene expression of DNA repair, apoptosis, and autophagy-related genes was analyzed by RT-PCR. Cell cycle distribution was determined using flow cytometry. Viability assays using MTT assay revealed IC50 values of 26 mM and 22.7 mM for SB and 6.77 μM, and 9.11 μM for CEL in LN-405 and T98G cells, respectively. Furthermore, we examined the expression levels of DNA repair genes (MGMT, MLH-1, MSH-2, MSH-6), apoptosis genes (caspase-3, caspase-8, caspase-9), and an autophagy gene (ATG-6) using real-time polymerase chain reaction. Additionally, flow cytometry analysis revealed alterations in cell cycle distribution following treatment with SB, CEL and their combination. These findings indicate that SB and CEL may act through multiple mechanisms, including DNA repair inhibition, apoptosis induction, and autophagy modulation, to exert their anti-cancer effects in glioblastoma cells. This is the first study providing novel insights into the potential therapeutic effects of SB and CEL in glioblastoma.

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