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Curcumin inhibits oral squamous cell carcinoma proliferation and invasion via EGFR signaling pathways
被引:2
|作者:
Zhen, Lei
[1
]
Fan, Desheng
[2
]
Yi, Xianghua
[2
]
Cao, Xinming
[1
]
Chen, Dong
[1
]
Wang, Liming
[1
]
机构:
[1] Shanghai Stomatol Dis Ctr, Dept Periodontol, Shanghai 200001, Peoples R China
[2] Tongji Univ, Shanghai Tongji Hosp, Dept Pathol, Shanghai 200065, Peoples R China
来源:
基金:
上海市自然科学基金;
关键词:
OSCC;
curcumin;
EGFR;
proliferation;
invasion;
GROWTH-FACTOR RECEPTOR;
BREAST-CANCER CELLS;
IN-VITRO;
CYCLE ARREST;
EXPRESSION;
CETUXIMAB;
APOPTOSIS;
COMBINATION;
ACTIVATION;
MIGRATION;
D O I:
暂无
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Epidermal growth factor receptor (EGFR) is an effective molecular target of anti-cancer therapies. Curcumin is known to inhibit growth, invasion and metastasis by downregulating EGFR expression in some cancer cells. However, the mechanism underlying the effect of curcumin in human oral squamous cell carcinoma (OSCC) remains unclear. In this study, we investigated the efficacy of curcumin on proliferation and invasion in SCC-25 cell line. We also explored the effect of curcumin on the activition of EGFR and its downstream signaling molecules Akt, ERK1/2 and STAT3. Furthermore, we examined the inhibition effect of curcumin on EGF-induced EGFR phosphorylation and SCC-25 cells invasion. Our results showed that curcumin inhibited SCC-25 cells proliferation and induced G2/M phase arrest in a dose-dependent manner. Curcumin also inhibited SCC-25 cells invasion and downregulated MMP-2, MMP-9, uPA and uPAR expression. We further revealed that curcumin regulated the p-EGFR and EGFR downstream signaling molecules including Akt, ERK1/2 and STAT3. Finally, our data showed that crucumin reduced the EGF-induced phosphorylation of EGFR and suppressed EGF-triggered SCC-25 cells invasion. Taken together, our results suggest that curcumin reduced SCC-25 cells proliferation and invasion through inhibiting the phosphorylation of EGFR and EGFR downstream signaling molecules Akt, ERK1/2 and STAT3.
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页码:6438 / 6446
页数:9
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