Health
New target discovered to overcome radioresistance in brain tumor cells
The current standard of care for glioblastoma (GBM), the most common and deadly primary tumor of the central nervous system, is radiation therapy after surgery and the chemotherapy drug temozolomide. GBM, a progressive brain tumor, is highly resistant to current therapies, has a high mortality rate, and recurs frequently. In addition, GBM cells are highly radioresistant and more actively contribute to tumor progression and recurrence if they survive radiotherapy. Therefore, there is an urgent need to modify standard therapeutic strategies and develop novel therapeutics to overcome the radioresistance of GBM cells.
To this end, a team of researchers from South Korea and the United States, led by Professor Boohyun Yoon of Busan National University, South Korea, explored the most important factors underlying radiation resistance in GBM cells, including the regulation of the internal steady state of lipids within the cell. revealed a plausible mechanism. “Lipid homeostasis”. “Simply put, radiation-tolerant GBM cells prefer to store fatty acids instead of utilizing them as an energy source in order to reduce mitochondrial reactive oxygen species. that It can damage DNA, RNA and proteins and cause cell death.explains Professor Yoon.
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In their study, published in cell report medicine, researchers took GBM stem cells from patients and established radiation-tolerant cells for investigation. They showed that diacylglycerol kinase B (DGKB), a regulator of intracellular levels of diacylglycerol (DAG), was significantly suppressed in radioresistant GBM cells. This increases DAG accumulation, reduces fatty acid oxidation, reduces mitochondrial lipotoxicity (accumulation of harmful lipids in non-adipose tissue) in GBM cells, and contributes to radiation resistance. showed that ionizing radiation induced increased levels of diacylglycerol acyltransferase 1 (DGAT1), an enzyme that catalyzes the formation of triglycerides from DAG.
Armed with this understanding, the researchers further demonstrated that genetic inhibition of DGAT1 suppressed radiation resistance. Furthermore, they found that the clinical drug cladribine activated her DGKB and inhibited DGAT1. This action sensitized GBM cells to radiotherapy. in vitro When live (mouse model).
“Our study has revealed cladribine as a radiosensitizer for GBM treatment by drug repurposing that can offer multiple benefits. ” says Professor Yoon. “As an FDA-approved oral drug, cladribine’s side effects are highly manageable and its pharmacokinetics are well-characterized. “Cladribine may become a standard future treatment for GBM.”
Taken together, this study indicates that DGKB and DGAT1 are potential therapeutic targets to overcome GBM radioresistance. Additionally, drugs like cladribine may replace existing treatment options with new, more effective strategies.
reference: Kang H, Lee H, Kim K et al. DGKB mediates radioresistance by modulating DGAT1-dependent lipotoxicity in glioblastoma. CR Med2023;4(1). Doi: 10.1016/j.xcrm.2022.100880
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