Downregulation of survivin by RNAi inhibits the growth of esophageal carcinoma cells

被引:62
作者
Wang, YH
Zhu, HX
Quan, LP
Zhou, CQ
Bai, JF
Zhang, G
Zhan, QM
Xu, NZ
机构
[1] Chinese Acad Med Sci, Inst Canc, Lab Cell & Mol Biol, Beijing 100021, Peoples R China
[2] Chinese Acad Med Sci, Canc Hosp, Beijing 100021, Peoples R China
[3] Peking Union Med Coll, Beijing 100021, Peoples R China
[4] Chinese Acad Med Sci, Inst Canc, Natl Lab Mol Oncol, Beijing 100021, Peoples R China
基金
中国国家自然科学基金;
关键词
survivin; esophageal cancer; RNA interference; apoptosis;
D O I
10.4161/cbt.4.9.1914
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Esophageal squamous cell carcinoma ranks among one of the most frequent cause of cancer death in the world. Understanding of the molecular mechanisms involved in the pathogenesis of esophageal cancer becomes critical to develop more effective treatments. Elevated expression of survivin in esophageal carcinoma has been reported before and suppression of survivin expression leads to many tumor cells growth inhibition. We hypothesized that downregulation of survivin would inhibit the growth of human esophageal cancer cells. RNA interference directed against survivin was introduced into a human esophageal squamous cell carcinoma cell line KYSE510. Stable clones were selected and western blot analysis was performed to detect the protein level of survivin. Tumor cell growth in vitro and in vivo was assessed by trypan blue exclusion and nude mice experiments. Annexin V/propidium iodide staining followed by flow cytometric analysis and TUNEL assay were used to detect apoptosis in cell culture and in nude mice. We found that RNA interference could efficiently and stably suppress survivin expression in KYSE510 cells. Downregulation of survivin resulted in significantly inhibition of tumor growth in vitro and in vivo. The mechanism appears to be increased induction of apoptosis. Our results suggest a potential role for the targeting of survivin in the treatments of esophageal carcinoma.
引用
收藏
页码:974 / 978
页数:5
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