Abstract
BackgroundBoron neutron capture therapy (BNCT) is a selective radiotherapy, being effective for the treatment of even advanced malignancies in head and neck regions as well as brain tumors and skin melanomas. To clarify the role of p53 gene, the effect of BNCT on oral squamous cell carcinoma (SCC) cells showing either wild- (SAS/neo) or mutant-type (SAS/mp53) p53 was examined.MethodsCells were exposed to neutron beams in the presence of boronophenylalanine (BPA) at Kyoto University Research Reactor. Treated cells were monitored for modulations in colony formation, proliferation, cell cycle, and expression of cell cycle-associated proteins.ResultsWhen SAS/neo and SAS/mp53 cells were subjected to BNCT, more suppressive effects on colony formation and cell viability were observed in SAS/neo compared with SAS/mp53 cells. Cell cycle arrest at the G1 checkpoint was observed in SAS/neo, but not in SAS/mp53. Apoptotic cells increased from 6 h after BNCT in SAS/neo and 48 h in SAS/mp53 cells. The expression of p21 was induced in SAS/neo only, but G2 arrest-associated proteins including Wee1, cdc2, and cyclin B1 were altered in both cell lines.ConclusionThese results indicate that oral SCC cells with mutant-type are more resistant to BNCT than those with wild-type p53, and that the lack of G1 arrest and related apoptosis may contribute to the resistance. At a physical dose affecting the cell cycle, BNCT inhibits oral SCC cells in p53-dependent and -independent manners.
Highlights
Boron neutron capture therapy (BNCT) is a selective radiotherapy, being effective for the treatment of even advanced malignancies in head and neck regions as well as brain tumors and skin melanomas
Boron neutron capture therapy (BNCT) is a binary modality: Boron-10 (10B)-enriched compounds such as boronophenylalanine (BPA) and borocaptate sodium are administered at first, followed by irradiation with thermal neutrons. 10B to captures thermal neutrons leads to the nuclear reaction 10B (n, α) 7Li
We examined the effects of BNCT on the proliferation, cell cycle, and cell cycle-related proteins of oral squamous cell carcinoma (SCC) cells showing wild- or mutant-type p53 with the same background and indicated the role of p53 in the suppressive effect of BNCT
Summary
Boron neutron capture therapy (BNCT) is a selective radiotherapy, being effective for the treatment of even advanced malignancies in head and neck regions as well as brain tumors and skin melanomas. Boron neutron capture therapy (BNCT) is a binary modality: Boron-10 (10B)-enriched compounds such as boronophenylalanine (BPA) and borocaptate sodium are administered at first, followed by irradiation with thermal neutrons. 10B to captures thermal neutrons leads to the nuclear reaction 10B (n, α) 7Li. Boron neutron capture therapy (BNCT) is a binary modality: Boron-10 (10B)-enriched compounds such as boronophenylalanine (BPA) and borocaptate sodium are administered at first, followed by irradiation with thermal neutrons. It has been shown that BNCT is effective for the treatment of advanced malignancies in head and neck regions as well as brain tumors and skin melanomas [9-12]
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