Academic Journal

Sulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model

التفاصيل البيبلوغرافية
العنوان: Sulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model
المؤلفون: Cho, Nam-Pyo, Han, Hye-Suk, Leem, Dae-Ho, Choi, In-Sun, Jung, Ji-Youn, Kim, Hyeong-Jin, Moon, Kyung-Suk, Choi, Kyeong-Hee, Soh, Yunjo, Kong, Gu, Cho, Sung Dae, Choi, Seoung Hwan
المساهمون: Cho, Sung Dae
بيانات النشر: Pergamon Press Ltd.
سنة النشر: 2024
المجموعة: Seoul National University: S-Space
مصطلحات موضوعية: NONSTEROIDAL ANTIINFLAMMATORY DRUGS, PROSTATE-CANCER CELLS, MEDIATED APOPTOSIS, TUMOR-GROWTH, CYCLE ARREST, OXIDATIVE STRESS, NECK-CANCER, IN-VIVO, HEAD, ISOTHIOCYANATE, Human oral squamous cell carcinoma, Sulforaphane, Apoptosis, COX-2, bcl-2, Xenograft
الوصف: In this study, we found that oral squamous cell carcinomas (OSCCs) in Korean patients have a high level of COX-2 expression when compared with normal mucosa. Sulforaphane (SFN), rich in cruciferous vegetables, has been reported to display anti-cancer activity against many cancers. However, the effect and molecular mechanism of SFN in the proliferation of OSCC still remains unclear. To elucidate this mechanism, we investigated the anti-proliferative effect of SFN on KB and YD-10B cells and demonstrated that SFN significantly induced caspase-dependent apoptosis. Also, we observed that SFN inhibited COX-2 but not COX-1. In addition, bcl-2 protein, one of downstream targets of COX-2, was down-regulated by SFN. Furthermore, SFN also inhibited tumor growth in KB cell xenografts. These results show that SFN can act as a potent anti-oral cancer compound by inhibiting COX-2 activity. (C) 2008 Elsevier Ltd. All rights reserved. ; N ; 1
نوع الوثيقة: article in journal/newspaper
اللغة: unknown
تدمد: 1368-8375
Relation: Oral Oncology, Vol.45 No.8, pp.654-660; https://hdl.handle.net/10371/208976; 000268112800002; 2-s2.0-67650401078; 221411
DOI: 10.1016/j.oraloncology.2008.07.003
الاتاحة: https://hdl.handle.net/10371/208976
https://doi.org/10.1016/j.oraloncology.2008.07.003
رقم الانضمام: edsbas.A35ADAC9
قاعدة البيانات: BASE
الوصف
تدمد:13688375
DOI:10.1016/j.oraloncology.2008.07.003