NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells
NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells
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NLK 是胆囊癌细胞增殖和迁移的关键调节因子
DOI：
10.1007/s11010-012-1365-0
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发表时间：
2012-10-01
影响因子：
4.3
通讯作者：
Liu, Yingbin
中科院分区：
文献类型：
--
作者：
Tan, Zhujun;Li, Maolan;Liu, Yingbin
胆囊癌（Gallbladder cancer，GBC）是世界上最致命的恶性肿瘤之一，在胃肠道恶性肿瘤中居第五位。胆囊癌的预后是非常可怕的部分原因是转移。因此，了解控制这种致命疾病转移的分子途径可能会为靶向治疗方法提供新的靶点。在这项研究中，我们研究了类线虫激酶（NLK）在GBC生长和迁移中的作用。采用慢病毒介导的siRNA来减轻GBC细胞系（GBC-SD和SGC-996）中NLK的表达水平。Real-time PCR和Western-blot分析表明，表达NLK-siRNA的慢病毒（Lv-shNLK）感染GBC-SD和SGC-996细胞后，NLK的mRNA和蛋白水平均降低。NLK低表达的GBC-SD和SGC-996细胞的增殖和体外成瘤（集落形成）能力以及迁移能力显著降低。我们的研究结果表明，NLK是GBC增殖和迁移的关键调节因子，它可以作为GBC的潜在治疗靶点。
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.