Sublocalization of Rab23, a mediator of Sonic hedgehog signaling pathway, in hepatocellular carcinoma cell lines

被引:17
|
作者
Sun, Hai-Ji [2 ,3 ]
Liu, Yun-Jian [1 ]
Li, Na [2 ]
Sun, Zhi-Yong [1 ]
Zhao, Hai-Wang [1 ]
Wang, Chen [1 ]
Li, Hui [1 ]
Ma, Fang-Ming [1 ]
Shi, Song-Mei [1 ]
Xu, Xiao-Qiu [1 ]
Chen, Zhe-Yu [2 ]
Huang, Shu-Hong [2 ]
机构
[1] Municipal Hosp Heze, Dept Hepatobiliary Surg, Heze, Shandong, Peoples R China
[2] Shandong Univ, Sch Med, Shandong Prov Key Lab Mental Disorders, Dept Neurobiol, Jinan 250012, Shandong, Peoples R China
[3] Shandong Normal Univ, Coll Life Sci, Jinan, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Rab23; hepatocellular carcinoma; Sonic hedgehog pathway; NEGATIVE REGULATOR; CARPENTER SYNDROME; SMALL GTPASES; MEMBRANE; PROTEINS; EXPRESSION; MECHANISM; TARGET; CANCER; BRAIN;
D O I
10.3892/mmr.2012.1094
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The novel member of the Rab family of GTPases, Rab23, is an essential negative regulator of the Sonic hedgehog (Shh) signaling pathway. Loss of function mutation of the Rab23 gene causes abnormal development of the neural tube in mice and in certain human congenital diseases. The aberrant overexpression of Rab23 has been associated with various diseases, such as gastric, hepatocellular and lung cancer. The exact function of Rab23 in hepatocellular carcinomas (HCCs), however, remains unknown. Previously, we reported the abnormal sublocalization of Rab23 in lung cancers. In the current study, we investigated the role of Rab23 in HCCs. We report the distinct sublocalization pattern of Rab23 in HCC cell lines. This difference depends on the GDP/GTP-binding form, and inhibition of the Rab23 cycle decreases the expression and nuclear localization of Glil.
引用
收藏
页码:1276 / 1280
页数:5
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