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MicroRNA-9 is a ponderable index for the prognosis of human hepatocellular carcinoma.
- Source :
-
International journal of clinical and experimental medicine [Int J Clin Exp Med] 2015 Oct 15; Vol. 8 (10), pp. 17748-56. Date of Electronic Publication: 2015 Oct 15 (Print Publication: 2015). - Publication Year :
- 2015
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Abstract
- Hepatocellular carcinoma (HCC) is one of the most common primary malignant tumors of the liver worldwide; however, despite its significance, there is a lack of treatment methods and clear prognoses. MicroRNA-9 (miR-9) is known to play an important role in tumor tumorigenesis and progression. Talin-1, which plays a significant role in regulating the transmutation of carcinoma, has been demonstrated to be downregulated by miR-9 in epithelial ovarian cancer. In the present study, we researched the potential role of miR-9 in the prognosis of HCC. The expression levels of miR-9 and Talin-1 mRNA in HCC tissues (n = 60), adjacent non-cancerous tissues (n = 60), and normal liver tissues (n = 20) were detected using a real-time quantitative assay; protein expression levels of Talin-1 were detected using western blot. The expression levels of miR-9 were significantly higher in HCC tissues (P < 0.001) than in normal liver and adjacent non-cancerous tissues. These levels were significantly associated with tumor grade, tumor size, portal vein tumor thrombus, integral capsule, and 2.0-year disease-free survival rate (P < 0.05). High levels of miR-9 were strongly associated with the malignant progression of HCC, and overexpression of miR-9 is a risk factor that has a statistically significant effect on survival rate. miR-9 could play a role as an HCC tumor activator by regulating the expression of Talin-1; therefore, miR-9 might be a potentially valuable biomarker for the prognosis in HCC patients.
Details
- Language :
- English
- ISSN :
- 1940-5901
- Volume :
- 8
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- International journal of clinical and experimental medicine
- Publication Type :
- Academic Journal
- Accession number :
- 26770365