Abstract
Radiotherapy is one of the remedies in the treatment of glioma. The radioresistance is a major drawback, of which the mechanism is unclear. Tribble protein and histone deacetylase are involved in the cancer pathogenesis. This study aims to test a hypothesis that the histone deacetylase inhibitors attenuate the radioresistance in human glioma cells. In this study, human glioma cells were cultured. The cells were treated with irradiation with or without a histone deacetylase inhibitor, butyrate. Apoptosis of the glioma cells was assessed by flow cytometry. The results showed that human glioma cells expressed a low level of Trib1, which was significantly up regulated by exposure to small doses (2 Gy/day for 4 days) of irradiation. Trib1-deficient glioma cells showed an enhanced response to irradiation-induced apoptosis. Exposure to small doses of irradiation, Trib1 formed a complex with pHDAC1 (phosphor histone deacetylase-1) to inhibit p53 expression in glioma cells. The presence of HDAC1 inhibitor, butyrate or parthenolide, significantly enforced irradiation-induced glioma cell apoptosis. In conclusion, the Trib1 plays a critical role in the development of radioresistance of glioma cells. The data suggest that inhibition of Trib1 or HDAC1 has the potential to prevent or attenuate the radioresistance.
Highlights
It is suggested that oral administration of probiotics improves the cancer symptoms and the life quality of cancer patients[10]
Based on the above information, we hypothesize that irradiation increases the expression of Trib[1] and HDAC1 in glioma cells, which can be prevented by the presence of butyrate
The data indicate that human glioma cells express Trib[1], which can be up regulated by irradiation, which may be associated with glioma cell activities in a radiation environment
Summary
It is suggested that oral administration of probiotics improves the cancer symptoms and the life quality of cancer patients[10]. Whether probiotics can play a role in modulating the development of the radioresistance has not been investigated. Some probiotics, such as Clostridium butyricum, can secret butyrate. Based on the above information, we hypothesize that irradiation increases the expression of Trib[1] and HDAC1 in glioma cells, which can be prevented by the presence of butyrate. The results showed that exposure to irradiation markedly increased the expression of Trib[1] in glioma cells, which was abolished by the presence of butyrate sodium. Butyrate inhibited the p53 expression in glioma cells and increased the irradiation-induced glioma cell apoptosis. The data suggest that administration of butyrate may prevent the development of radioprotention in glioma cells during radiotherapy
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