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Role of p53 mutation in the effect of boron neutron capture therapy on oral squamous cell carcinoma.

Fujita Y, Kato I, Iwai S, Ono K, Suzuki M, Sakurai Y, Ohnishi K, Ohnishi T, Yura Y - Radiat Oncol (2009)

Bottom Line: When 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.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.These 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Oral and Maxillofacial Surgery, Osaka University Graduate School of Dentistry, Osaka, Japan. fujisan@dent.osaka-u.ac.jp

ABSTRACT

Background: 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. 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.

Methods: Cells 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.

Results: When 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.

Conclusion: These 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.

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Related in: MedlinePlus

Suppression of the colony formation of oral SCC cells by BNCT. SAS/neo and SAS/mp53 cells were treated with BNCT, and survival fractions were assessed based on colony formation.
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Figure 1: Suppression of the colony formation of oral SCC cells by BNCT. SAS/neo and SAS/mp53 cells were treated with BNCT, and survival fractions were assessed based on colony formation.

Mentions: SAS/neo and SAS/mp53 cells were treated with BNCT, and the survival ratios were calculated based on colony formation. In both cell lines, the survival ratios decreased in a dose-dependent manner, but SAS/neo were suppressed more strongly than SAS/mp53 cells. At a dose of 6 Gy, the survival fractions of SAS/neo and SAS/mp53 cells were 8 and 36%, respectively (Figure 1).


Role of p53 mutation in the effect of boron neutron capture therapy on oral squamous cell carcinoma.

Fujita Y, Kato I, Iwai S, Ono K, Suzuki M, Sakurai Y, Ohnishi K, Ohnishi T, Yura Y - Radiat Oncol (2009)

Suppression of the colony formation of oral SCC cells by BNCT. SAS/neo and SAS/mp53 cells were treated with BNCT, and survival fractions were assessed based on colony formation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2803486&req=5

Figure 1: Suppression of the colony formation of oral SCC cells by BNCT. SAS/neo and SAS/mp53 cells were treated with BNCT, and survival fractions were assessed based on colony formation.
Mentions: SAS/neo and SAS/mp53 cells were treated with BNCT, and the survival ratios were calculated based on colony formation. In both cell lines, the survival ratios decreased in a dose-dependent manner, but SAS/neo were suppressed more strongly than SAS/mp53 cells. At a dose of 6 Gy, the survival fractions of SAS/neo and SAS/mp53 cells were 8 and 36%, respectively (Figure 1).

Bottom Line: When 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.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.These 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Oral and Maxillofacial Surgery, Osaka University Graduate School of Dentistry, Osaka, Japan. fujisan@dent.osaka-u.ac.jp

ABSTRACT

Background: 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. 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.

Methods: Cells 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.

Results: When 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.

Conclusion: These 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.

Show MeSH
Related in: MedlinePlus