ArticleMolecular and cellular biochemistry2012
NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Tissue fluidity mediated by adherens junction dynamics promotes planar cell polarity-driven ommatidial rotation.Nature communications · 2021Article
- Expression of Nemo-like kinase in cervical squamous cell carcinoma: a clinicopathological study.OncoTargets and therapy · 2018Article
- ZNF148 modulates TOP2A expression and cell proliferation via ceRNA regulatory mechanism in colorectal cancer.Medicine · 2017Article
- Up-regulation of PKM2 promote malignancy and related to adverse prognostic risk factor in human gallbladder cancer.Scientific reports · 2016Article
- Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells.Scientific reports · 2016Article
- Lentivirus-mediated knockdown of NLK inhibits small-cell lung cancer growth and metastasis.Drug design, development and therapy · 2016Article
- The emerging role of Nemo-like kinase (NLK) in the regulation of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Prognostic significance of Nemo-like kinase expression in patients with hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- NLK functions to maintain proliferation and stemness of NSCLC and is a target of metformin.Journal of hematology & oncology · 2015Article
- Lentivirus‑delivered nemo‑like kinase small interfering RNA inhibits laryngeal cancer cell proliferation in vitro.Molecular medicine reports · 2015Article
- Upregulation of nemo-like kinase is an independent prognostic factor in colorectal cancer.World journal of gastroenterology · 2015Article
- SPOCK1 as a potential cancer prognostic marker promotes the proliferation and metastasis of gallbladder cancer cells by activating the PI3K/AKT pathway.Molecular cancer · 2015Article
- Control of stem cell self-renewal and differentiation by the heterochronic genes and the cellular asymmetry machinery in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Long Noncoding RNA KIAA0125 Potentiates Cell Migration and Invasion in Gallbladder Cancer.BioMed research international · 2015Article
- Expression of Nemo-like kinase was increased and negatively correlated with the expression of TCF4 in lung cancers.International journal of clinical and experimental pathology · 2015Article
- Zinc finger X-chromosomal protein (ZFX) is a significant prognostic indicator and promotes cellular malignant potential in gallbladder cancer.Cancer biology & therapy · 2015Article
- Article
- RETRACTED: Schisandrin B induces apoptosis and cell cycle arrest of gallbladder cancer cells.Molecules (Basel, Switzerland) · 2014Article
- MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway.Cancer biology & therapy · 2014Article
- Triptolide induces s phase arrest and apoptosis in gallbladder cancer cells.Molecules (Basel, Switzerland) · 2014Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.