RAB23, regulated by miR-92b, promotes the progression of esophageal squamous cell carcinoma

被引：21

作者：

Cheng, Lina ^{[1
]}

Yang, Fan ^{[1
]}

Zhou, Bingxi ^{[1
]}

Yang, Hui ^{[1
]}

Yuan, Yuan ^{[1
]}

Li, Xiuling ^{[1
]}

Han, Shuangyin ^{[1
]}

机构：

[1] Zhengzhou Univ, Peoples Hosp, Henan Prov Peoples Hosp, Dept Gastroenterol, 7th Weiwu Rd, Zhengzhou 450003, Henan Province, Peoples R China

来源：

GENE | 2016年 / 595卷 / 01期

关键词：

RAB23; ESCC; Cell growth and migration; Beta-catenin/TCF signaling; miR-92b; TARGETS MULTIPLE MEMBERS; CANCER STATISTICS; PROGNOSTIC-FACTOR; INVASION; MIR-200B;

D O I：

10.1016/j.gene.2016.09.028

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

RAB23, a member of Ras-related small GTPase family, has been reported to be up-regulated in several cancer types. However, its biological functions and the underlying molecular mechanisms for its oncogenic roles in esophageal squamous cell carcinoma (ESCC) remain unknown. In this study, we have shown that the expression of RAB23 was elevated in ESCC tissues and ESCC cells. Overexpression of RAB23 promoted the growth and migration of the ESCC cells, while knocking down the expression RAB23 inhibited the growth, migration and metastasis of the ESCC cells. The molecular mechanism study showed that RAB23 activated beta-cateniniTCF signaling and regulated the expression of several target genes. In the further study, it was found that the expression of RAB23 was regulated by the miR-92b. Forced expression of MiR-92b decreased the mRNA and protein level of RAB23, and RAB23 rescued the biological functions of miR-92b. Taken together, this study revealed the oncogenic roles and the regulation of RAB23 in ESCC, suggesting RAB23 might be a therapeutic target. (C) 2016 Published by Elsevier B.V.

引用

页码：31 / 38

页数：8

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