NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells

被引：41

作者：

Tan, Zhujun ^{[1
]}

Li, Maolan ^{[1
]}

Wu, Wenguang ^{[1
]}

Zhang, Lin ^{[1
]}

Ding, Qichen ^{[1
]}

Wu, Xiangsong ^{[1
]}

Mu, Jiasheng ^{[1
]}

Liu, Yingbin ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Xinhua Hosp, Sch Med, Dept Gen Surg, Shanghai 200092, Peoples R China

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2012年 / 369卷 / 1-2期

关键词：

Gallbladder carcinoma; Nemo-like kinase; Migration; Proliferation; NEMO-LIKE KINASE; INDUCTION; PATHWAY; GROWTH; CANCER;

D O I：

10.1007/s11010-012-1365-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Gallbladder cancer (GBC) is one of the most lethal neoplasm and is the fifth most common malignancy of gastrointestinal tract. The prognosis of gallbladder cancer is extremely terrible partially due to metastasis. Thus, understanding the molecular pathways controlling metastasis of this lethal disease may provide new targets for targeted therapeutic approach. In this study, we investigated the function of nemo-like kinase (NLK) in GBC growth and migration. Lentivirus-mediated siRNA was employed to alleviate the expression level of NLK in GBC cell lines (GBC-SD and SGC-996). Real-time PCR and western-blot analysis demonstrated that both mRNA and protein levels of NLK in GBC-SD and SGC-996 cells were decreased after infection with NLK-siRNA-expressing lentivirus (Lv-shNLK). The proliferation and in vitro tumorigenesis (colony formation) ability as well as migration of GBC-SD and SGC-996 cells with low NLK expression decreased significantly. Our results suggested that NLK is a key regulator involved in proliferation and migration of GBC, and it could be used as a potential therapeutic target for GBC.

引用

页码：27 / 33

页数：7

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