SQLE induces epithelial-to-mesenchymal transition by regulating of miR-133b in esophageal squamous cell carcinoma

被引:38
|
作者
Qin, Yi [1 ]
Zhang, Yi [2 ]
Tang, Qinting [3 ]
Jin, Li [4 ]
Chen, Yong'an [2 ]
机构
[1] First Peoples Hosp Yancheng City, Dept Gastroenterol, Yancheng 224001, Peoples R China
[2] Jimin Hosp, Dept Oncol, Shanghai 200052, Peoples R China
[3] Yancheng Vocat Inst Hlth Sci, Coll Nursing, Yancheng 224006, Peoples R China
[4] Sichuan Canc Hosp, Chengdu 610041, Peoples R China
关键词
esophageal squamous cell carcinoma; miR-133b; SQLE; epithelial-to-mesenchymal transition; SQUALENE EPOXIDASE; EXPRESSION; GENES; MICRORNAS; TARGET; GROWTH;
D O I
10.1093/abbs/gmw127
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
Increasing evidence suggests that microRNAs, which control gene expression at the post-transcriptional level, are aberrantly expressed in cancers and play significant roles in carcinogenesis and cancer progression. In this study, we show differential miR-133b down-expression in human esophageal squamous cell carcinoma (ESCC) cells and tissues. In addition, squalene epoxidase (SQLE), a key enzyme of cholesterol synthesis, is identified as the direct downstream target gene of miR-133b by luciferase gene reporter assay. Furthermore, ectogenic miR-133b expression and SQLE knockdown can inhibit proliferation, invasion, and metastasis, and diminish epithelial-to- mesenchymal transition (EMT) traits of ESCC in vitro, implying that miR-133b-dependent SQLE can induce tumorigenicity and that SQLE is an EMT inducer. Xenograft experiment results also proved the biological function of SQLE in vivo. Therefore, we conclude that miR-133b-dependent SQLE plays a critical role in the potential metastasis mechanisms in ESCC.
引用
收藏
页码:138 / 148
页数:11
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