Abstract:
:Inactivation of antineoplastics is a serious problem in cancer therapy, and prevention of the inactivation is a surpassing strategy for enhancement of their therapeutic effects. BOF-A2, which contains both EM-FU, a masked form of 5-fluorouracil (5-FU), and CNDP, an inhibitor of 5-FU degradation, was developed with this aim. We compared the antitumor effects of BOF-A2 and 5-FU in human squamous cell carcinoma cells transplanted to nu/nu mice. Each drug (0.9-7.0 mg/kg of 5-FU and 3.8-30 mg/kg of BOF-A2) was orally administered every day to 5 mice in each dosage group for 4 weeks. Although the maximal tumor growth inhibition by 5-FU (3.5 mg/kg per day) was about 50% of the control value, 15 mg/kg per day of BOF-A2, which is equimolar to 3.5 mg/kg per day of 5-FU, almost completely inhibited the tumor growth. The flow-cytometric analysis revealed that BOF-A2 (15 mg/kg per day) induced more prominent S-phase-accumulation (63 +/- 6%) of tumor cells than did 3.5 mg/kg per day of 5-FU (43 +/- 18%), and immunohistochemical stainings indicated that the decrease of proliferating cell nuclear antigen expression was more prominent in tumor cells in the BOF-A2-treated mice than in the 5-FU-treated mice. Correspondingly, the DNA synthesis was markedly suppressed in tumor cells obtained from BOF-A2-treated mice. Compared with 5-FU, BOF-A2 more strongly induced apoptosis; apoptotic cells detected by nick-end labeling techniques were about 20% of the tumor cells in 5-FU (3.5 mg/kg per day)-treated mice, and nearly 50% in BOF-A2 (15 mg/kg per day)-administered mice. The expressions of involucrin, cytokeratin 10 and protein kinase C eta, which are associated with squamous cell differentiation, were not increased by BOF-A2 or 5-FU, although the expression of transglutaminase was slightly augmented by both drugs. These results indicate that compared with 5-FU, BOF-A2 more strongly suppresses the growth of squamous cell carcinoma by inhibiting DNA synthesis and inducing apoptosis but not cell differentiation.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Yoneda K,Yamamoto T,Ueta E,Osaki Tdoi
10.1016/s0304-3835(98)00330-9keywords:
subject
Has Abstractpub_date
1999-03-22 00:00:00pages
17-25issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(98)00330-9journal_volume
137pub_type
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