共 50 条
MDA-7/IL-24 inhibits cell survival by inducing apoptosis in nasopharyngeal carcinoma
被引:2
|作者:
Lin, Cheng
[2
]
Liu, Haibin
[1
]
Li, Li
[1
]
Zhu, Qiubei
[1
]
Liu, Huanhai
[1
]
Ji, Zhenghua
[1
]
Liao, Jianchun
[1
]
Lang, Juntian
[1
]
Wu, Jian
[1
]
Fan, Jingping
[1
]
机构:
[1] Second Mil Med Univ, Changzheng Hosp, Dept Otolaryngol Head & Neck Surg, Shanghai 200003, Peoples R China
[2] 452 Hosp, Dept Otolaryngol Head & Neck Surg, Chengdu 610021 1, Peoples R China
来源:
关键词:
MDA-7/IL-24;
nasopharyngeal carcinoma;
cell survival;
DIFFERENTIATION-ASSOCIATED GENE-7;
MELANOMA-DIFFERENTIATION;
TUMOR-SUPPRESSOR;
CANCER CELLS;
XENOGRAFT TUMORS;
MDA-7;
GENE;
PHASE-I;
EXPRESSION;
FAMILY;
GROWTH;
D O I:
暂无
中图分类号:
R-3 [医学研究方法];
R3 [基础医学];
学科分类号:
1001 ;
摘要:
Aims: Nasopharyngeal carcinoma (NPC) is the most common primary malignancy of the nasopharynx. Due to its local recurrence and distant metastasis, conventional therapy is usually ineffective. MDA-7/IL-24 (melanoma differentiation associated gene 7), a member of the IL10 family of cytokines, inhibits growth of various human cancer cells, but the underlying mechanism is largely unknown. There is no report of mda-7 in nasopharyngeal carcinoma. We aimed to investigate the role of MDA-7/IL-24 in NPC. Methods: Immune defective adenoviral vector carrying the gene was produced, infected NPC CNE cells and observed its growth, cell proliferation, apoptosis and the effect of combination with chemotherapy. Results: The results showed that (1) MDA-7/IL-24 inhibited NPC CNE cell growth and survival; (2) mda-7 induced cell apoptosis and death; (3) MDA-7/IL-24 in collaboration with chemotherapy induced cell apoptosis significantly; (4) MDA-7/IL-24 induced cell apoptosis by down-regulation of anti-apoptosis molecules such as Bcl-2 and Bcl-xl and up-regulation of caspase 3. Conclusion: The results suggested that MDA-7/IL-24 had obvious therapeutic effect in NPC cells. It is verified that adenovirus mediated MDA-7/IL-24 represents a potentially important new approach to NPC therapy.
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页码:4082 / 4090
页数:9
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