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MicroRNA-133b inhibits the growth of non-small-cell lung cancer by targeting the epidermal growth factor receptor
被引:92
|作者:
Liu, Lingxiang
[1
]
Shao, Xiaoyan
[2
]
Gao, Wen
[1
]
Zhang, Zhi
[3
]
Liu, Ping
[1
]
Wang, Rongsheng
[1
]
Huang, Puwen
[1
]
Yin, Yongmei
[1
]
Shu, Yongqian
[1
]
机构:
[1] Nanjing Med Univ, Affiliated Hosp 1, Ctr Canc, Nanjing, Jiangsu, Peoples R China
[2] Nanjing Univ, Sch Med, Affiliated DrumTower Hosp, Dept Hematol, Nanjing, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Canc Hosp, Dept Thorac Surg, Nanjing, Jiangsu, Peoples R China
基金:
中国国家自然科学基金;
关键词:
epidermal growth factor receptor (EGFR);
microRNA;
miR-133b;
non-small-cell lung cancer;
targeted therapy;
DIFFERENTIAL EXPRESSION;
CLINICAL-RESPONSE;
EGFR EXPRESSION;
COPY NUMBER;
IN-VITRO;
GEFITINIB;
MIR-133B;
SURVIVAL;
GENE;
MUTATIONS;
D O I:
10.1111/j.1742-4658.2012.08741.x
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Both the deregulation of microRNAs and epidermal growth factor receptor (EGFR) are emerging as important factors in non-small-cell lung cancer (NSCLC). Here, miR-133b was found to be associated with tumor stage, the extent of regional lymph node involvement, stage, visceral pleura or vessel invasion and EGFR mRNA expression in Chinese patients with NSCLC. Bioinformatic analysis and luciferase reporter assay revealed that miR-133b can interact specifically with the 3'-UTR of EGFR mRNA. Functionally, miR-133b transfection showed regulatory activity in translationally repressing EGFR mRNA. Moreover, miR-133b transfection may modulate apoptosis, invasion and sensitivity to EGFR-TKI through the EGFR signaling pathways, especially in EGFR-addicted NSCLC cells. Taken together, our findings show that miR-133b can inhibit cell growth of NSCLC through targeting EGFR and regulating its downstream signaling pathway. This finding has important implications for the development of targeted therapeutics for a number of EGFR-addicted cancers.
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页码:3800 / 3812
页数:13
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