| Literature DB >> 24189458 |
Qingyu Shen1, Hyun Jin Bae1, Jung Woo Eun1, Hyung Seok Kim1, Se Jin Park1, Woo Chan Shin1, Eun Kyung Lee2, Soha Park3, Won Sang Park1, Jung Young Lee1, Suk Woo Nam4.
Abstract
Nemo-like kinase (NLK), an evolutionarily conserved MAP kinase-related kinase, has been reported to be involved in the development of hepatocellular carcinoma (HCC), but the underlying mechanisms leading to oncogenic NLK are poorly understood. A comprehensive microRNA (miRNA) profiling analysis on human HCC tissues identified four downregulated miRNAs that may target NLK. Ectopic expression of miRNA mimics suggested that miR-101 could suppress NLK in HCC cells. Notably, ectopic miR-101 expression repressed cancer cell growth and proliferation and imitated NLK knockdown effect on HCC cells. In conclusion, we suggest that miR-101 functions as a tumor suppressor by regulating abnormal NLK activity in liver.Entities:
Keywords: Liver cancer; MiR-101; NLK; Tumor suppressor
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Year: 2013 PMID: 24189458 DOI: 10.1016/j.canlet.2013.10.030
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679