Abstract

The purpose of this study was to investigate the chemopreventive effect of carotenoids on proliferating cell nuclear antigen (PCNA) and cyclin D1 expression in betel (Areca catechu) quid extract (BQE)-induced hamster oral cancer and human KB cell models, respectively. In the in vivo animal study, 41 hamsters were divided into six groups and treated with 0.3 ml of 0.5% 9,10-dimethyl-1,2-benz[a]-anthracene, BQE, α-tocopherol, β-carotene, lycopene, lutein and mixed carotenoids for 12 weeks. After treatment, the pouches were excised and graded using an immunohistochemical assay of PCNA. In the in vitro cell experiment, KB cells were cultured, and the inhibitory effect of carotenoids (β-carotene, lycopene and lutein) on cell proliferation was evaluated. Cyclin D1 and PCNA were evaluated in terms of cell differentiation. In the results, most of the animal lesions showed no overexpression of PCNA. However, in dysplastic lesions, PCNA expressions by the β-carotene, lutein, lycopene, mixed and vitamin E groups were less than that of the control group. In papilloma lesions, PCNA expressions by the β-carotene, mixed and vitamin E groups were less severe than that of the control group. PCNA expression by the vitamin E-treated group was less severe than that of the control group. No carcinoma was found in the lycopene or mixed groups. In the cell study, all carotenoids exerted a significant inhibitory effect on KB cell proliferation. Although lycopene suppressed KB cell proliferation at the G0/G1 phase with a significant decrease in PCNA expression, β-carotene and lutein possessed less of an inhibitory effect and even exhibited elevated cell proliferation at the G2/M phase. These results indicate that different carotenoids present various suppressive abilities against PCNA and cyclin D1 expressions in cell proliferation. In conclusion, carotenoids suppressed the carcinogenesis of induced hamster oral cancer and a cancer cell line by acting as a suppressor which inhibited the expressions of PCNA and cyclin D1.

Original languageEnglish
Pages (from-to)667-675
Number of pages9
JournalJournal of Nutritional Biochemistry
Volume18
Issue number10
DOIs
Publication statusPublished - Oct 2007

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Cyclin D1
Proliferating Cell Nuclear Antigen
Carotenoids
Cell proliferation
KB Cells
Lutein
Cell Proliferation
Vitamin E
Cricetinae
Mouth Neoplasms
Control Groups
Animals
Areca
Luteal Cells
Cell Cycle Resting Phase
Tocopherols
G2 Phase
G1 Phase
Papilloma
Cell Division

Keywords

  • Betel quid extract
  • Carotenoids
  • Cyclin D
  • Oral cancer
  • Proliferating cell nuclear antigen

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Carotenoids suppress proliferating cell nuclear antigen and cyclin D1 expression in oral carcinogenic models. / Cheng, Hsin Chung; Chien, Hsin; Liao, Chia Hui; Yang, Yi Yuan; Huang, Shih Yi.

In: Journal of Nutritional Biochemistry, Vol. 18, No. 10, 10.2007, p. 667-675.

Research output: Contribution to journalArticle

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abstract = "The purpose of this study was to investigate the chemopreventive effect of carotenoids on proliferating cell nuclear antigen (PCNA) and cyclin D1 expression in betel (Areca catechu) quid extract (BQE)-induced hamster oral cancer and human KB cell models, respectively. In the in vivo animal study, 41 hamsters were divided into six groups and treated with 0.3 ml of 0.5{\%} 9,10-dimethyl-1,2-benz[a]-anthracene, BQE, α-tocopherol, β-carotene, lycopene, lutein and mixed carotenoids for 12 weeks. After treatment, the pouches were excised and graded using an immunohistochemical assay of PCNA. In the in vitro cell experiment, KB cells were cultured, and the inhibitory effect of carotenoids (β-carotene, lycopene and lutein) on cell proliferation was evaluated. Cyclin D1 and PCNA were evaluated in terms of cell differentiation. In the results, most of the animal lesions showed no overexpression of PCNA. However, in dysplastic lesions, PCNA expressions by the β-carotene, lutein, lycopene, mixed and vitamin E groups were less than that of the control group. In papilloma lesions, PCNA expressions by the β-carotene, mixed and vitamin E groups were less severe than that of the control group. PCNA expression by the vitamin E-treated group was less severe than that of the control group. No carcinoma was found in the lycopene or mixed groups. In the cell study, all carotenoids exerted a significant inhibitory effect on KB cell proliferation. Although lycopene suppressed KB cell proliferation at the G0/G1 phase with a significant decrease in PCNA expression, β-carotene and lutein possessed less of an inhibitory effect and even exhibited elevated cell proliferation at the G2/M phase. These results indicate that different carotenoids present various suppressive abilities against PCNA and cyclin D1 expressions in cell proliferation. In conclusion, carotenoids suppressed the carcinogenesis of induced hamster oral cancer and a cancer cell line by acting as a suppressor which inhibited the expressions of PCNA and cyclin D1.",
keywords = "Betel quid extract, Carotenoids, Cyclin D, Oral cancer, Proliferating cell nuclear antigen",
author = "Cheng, {Hsin Chung} and Hsin Chien and Liao, {Chia Hui} and Yang, {Yi Yuan} and Huang, {Shih Yi}",
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AU - Chien, Hsin

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AU - Yang, Yi Yuan

AU - Huang, Shih Yi

PY - 2007/10

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N2 - The purpose of this study was to investigate the chemopreventive effect of carotenoids on proliferating cell nuclear antigen (PCNA) and cyclin D1 expression in betel (Areca catechu) quid extract (BQE)-induced hamster oral cancer and human KB cell models, respectively. In the in vivo animal study, 41 hamsters were divided into six groups and treated with 0.3 ml of 0.5% 9,10-dimethyl-1,2-benz[a]-anthracene, BQE, α-tocopherol, β-carotene, lycopene, lutein and mixed carotenoids for 12 weeks. After treatment, the pouches were excised and graded using an immunohistochemical assay of PCNA. In the in vitro cell experiment, KB cells were cultured, and the inhibitory effect of carotenoids (β-carotene, lycopene and lutein) on cell proliferation was evaluated. Cyclin D1 and PCNA were evaluated in terms of cell differentiation. In the results, most of the animal lesions showed no overexpression of PCNA. However, in dysplastic lesions, PCNA expressions by the β-carotene, lutein, lycopene, mixed and vitamin E groups were less than that of the control group. In papilloma lesions, PCNA expressions by the β-carotene, mixed and vitamin E groups were less severe than that of the control group. PCNA expression by the vitamin E-treated group was less severe than that of the control group. No carcinoma was found in the lycopene or mixed groups. In the cell study, all carotenoids exerted a significant inhibitory effect on KB cell proliferation. Although lycopene suppressed KB cell proliferation at the G0/G1 phase with a significant decrease in PCNA expression, β-carotene and lutein possessed less of an inhibitory effect and even exhibited elevated cell proliferation at the G2/M phase. These results indicate that different carotenoids present various suppressive abilities against PCNA and cyclin D1 expressions in cell proliferation. In conclusion, carotenoids suppressed the carcinogenesis of induced hamster oral cancer and a cancer cell line by acting as a suppressor which inhibited the expressions of PCNA and cyclin D1.

AB - The purpose of this study was to investigate the chemopreventive effect of carotenoids on proliferating cell nuclear antigen (PCNA) and cyclin D1 expression in betel (Areca catechu) quid extract (BQE)-induced hamster oral cancer and human KB cell models, respectively. In the in vivo animal study, 41 hamsters were divided into six groups and treated with 0.3 ml of 0.5% 9,10-dimethyl-1,2-benz[a]-anthracene, BQE, α-tocopherol, β-carotene, lycopene, lutein and mixed carotenoids for 12 weeks. After treatment, the pouches were excised and graded using an immunohistochemical assay of PCNA. In the in vitro cell experiment, KB cells were cultured, and the inhibitory effect of carotenoids (β-carotene, lycopene and lutein) on cell proliferation was evaluated. Cyclin D1 and PCNA were evaluated in terms of cell differentiation. In the results, most of the animal lesions showed no overexpression of PCNA. However, in dysplastic lesions, PCNA expressions by the β-carotene, lutein, lycopene, mixed and vitamin E groups were less than that of the control group. In papilloma lesions, PCNA expressions by the β-carotene, mixed and vitamin E groups were less severe than that of the control group. PCNA expression by the vitamin E-treated group was less severe than that of the control group. No carcinoma was found in the lycopene or mixed groups. In the cell study, all carotenoids exerted a significant inhibitory effect on KB cell proliferation. Although lycopene suppressed KB cell proliferation at the G0/G1 phase with a significant decrease in PCNA expression, β-carotene and lutein possessed less of an inhibitory effect and even exhibited elevated cell proliferation at the G2/M phase. These results indicate that different carotenoids present various suppressive abilities against PCNA and cyclin D1 expressions in cell proliferation. In conclusion, carotenoids suppressed the carcinogenesis of induced hamster oral cancer and a cancer cell line by acting as a suppressor which inhibited the expressions of PCNA and cyclin D1.

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