Chemopreventive effects of pterostilbene through p53 and cell cycle in mouse lung of squamous cell carcinoma model
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作者:
Omchit Surien
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机构:Universiti Kebangsaan Malaysia (UKM),Programme of Biomedical Science, Center for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences
Omchit Surien
Ahmad Rohi Ghazali
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机构:Universiti Kebangsaan Malaysia (UKM),Programme of Biomedical Science, Center for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences
Ahmad Rohi Ghazali
Siti Fathiah Masre
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机构:Universiti Kebangsaan Malaysia (UKM),Programme of Biomedical Science, Center for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences
Siti Fathiah Masre
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[1] Universiti Kebangsaan Malaysia (UKM),Programme of Biomedical Science, Center for Toxicology and Health Risk Studies (CORE), Faculty of Health Sciences
Cell proliferation and cell death abnormalities are strongly linked to the development of cancer, including lung cancer. The purpose of this study was to investigate the effect of pterostilbene on cell proliferation and cell death via cell cycle arrest during the transition from G1 to S phase and the p53 pathway. A total of 24 female Balb/C mice were randomly categorized into four groups (n = 6): N-nitroso-tris-chloroethyl urea (NTCU) induced SCC of the lungs, vehicle control, low dose of 10 mg/kg PS + NTCU (PS10), and high dose of 50 mg/kg PS + NTCU (PS50). At week 26, all lungs were harvested for immunohistochemistry and Western blotting analysis. Ki-67 expression is significantly lower, while caspase-3 expression is significantly higher in PS10 and PS50 as compared to the NTCU (p < 0.05). There was a significant decrease in cyclin D1 and cyclin E2 protein expression in PS10 and PS50 when compared to the NTCU (p < 0.05). PS50 significantly increased p53, p21, and p27 protein expression when compared to NTCU (p < 0.05). Pterostilbene is a potential chemoprevention agent for lung SCC as it has the ability to upregulate the p53/p21 pathway, causing cell cycle arrest.
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, Malaysia
Surien, Omchit
Ghazali, Ahmad Rohi
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, Malaysia
Ghazali, Ahmad Rohi
Masre, Siti Fathiah
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Programme Biomed Sci, Kuala Lumpur, Malaysia
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, Malaysia
Surien, Omchit
Masre, Siti Fathiah
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, Malaysia
Masre, Siti Fathiah
Basri, Dayang Fredalina
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Diagnost Therapeut & Investigat Studies CODTI, Kuala Lumpur 50300, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, Malaysia
Basri, Dayang Fredalina
Ghazali, Ahmad Rohi
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Univ Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, MalaysiaUniv Kebangsaan Malaysia UKM, Fac Hlth Sci, Ctr Toxicol & Hlth Risk Studies CORE, Kuala Lumpur 50300, Malaysia