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Title: MiR-21 promoted proliferation and migration in hepatocellular carcinoma through negative regulation of Navigator-3

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [3]
  1. The Digestive and Vascural Surgery Center, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region (China)
  2. The Department of Liver and Biliary Pancreatic Surgery, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region (China)
  3. The Department of General Surgery, Branching Hospital of the First People's Hospital of Urumqi, 830000, Xinjiang Uygur Autonomous Region (China)

MicroRNA-21 (miR-21) has been well-established and found to be over-expressed in various human cancers and has been associated with hepatocellular carcinoma (HCC) progression. However, the underlying mechanism of miR-21 involvement in the development and progression of HCC remains to be understood. In the present study, we firstly identified that the Navigator-3 (NAV-3) gene as a novel direct target of miR-21. Knock-down of NAV-3 using shRNA can rescue the effects of anti-miR-21 inhibitor in HCC cell lines, whereas re-expression of miR-21 using transfection with miR-21 mimics phenocopied the NAV-3 knock-down model. Additionally, miR-21 levels inversely correlated with NAV-3 both in HCC cells and tissues. Knock-down of NAV-3 promoted both the proliferation and migration in HCC cells. Together, our findings suggest an important role for miR-21 in the progression of HCC, which negatively regulated Navigator-3 in the migration of HCC. - Highlights: • Navigator-3 (NAV-3) suppresses proliferation, migration and tumorigenesis of HCC cells. • NAV-3 was a novel target of miR-21. • MiR-21 negatively regulates NAV-3 in HCC.

OSTI ID:
22462242
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 464, Issue 4; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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