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

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A Correction to this article was published on 05 October 2021

An Erratum to this article was published on 18 July 2012

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Abstract

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.

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Correspondence to Yingbin Liu.

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11010_2012_1365_MOESM1_ESM.tif

Figure S1. Expression of NLK gene in GBC cell lines, GBC-SD and SGC-996. A. Analysis of NLK mRNA in both GBC cell lines by using quantitative real-time PCR assay. B. Analysis of NLK protein in both GBC cell lines by using western blot assay. (TIFF 227 kb)

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Tan, Z., Li, M., Wu, W. et al. NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells. Mol Cell Biochem 369, 27–33 (2012). https://doi.org/10.1007/s11010-012-1365-0

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  • DOI: https://doi.org/10.1007/s11010-012-1365-0

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