@Article{096504018X15201143705855,
AUTHOR = {Genglong Zhu, Xialei Liu, Yonghui Su, Fangen Kong, Xiaopeng Hong, Zhidong Lin},
TITLE = {Knockdown of Urothelial Carcinoma-Associated 1 Suppressed  Cell Growth and Migration Through Regulating miR-301a and  CXCR4 in Osteosarcoma MHCC97 Cells},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {1},
PAGES = {55--64},
URL = {http://www.techscience.com/or/v27n1/48660},
ISSN = {1555-3906},
ABSTRACT = {Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various 
cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in 
cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression 
of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and 
CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell 
viability, migration, invasion, and apoptosis were assessed. The results revealed that UCA1 expression was 
relatively higher in MHCC97 cells than in MG63, hFOB1.19, and OS-732 cells. Knockdown of UCA1 reduced 
cell viability, inhibited migration and invasion, and promoted cell apoptosis. However, the effect of UCA1 
knockdown on cell growth and migration was blocked by miR-301a overexpression, whose expression was 
regulated by UCA1. We also found that miR-301a positively regulated CXCR4 expression. CXCR4 inhibition 
reversed the effect of miR-301a overexpression on cell growth and migration. Moreover, miR-301a activated 
the Wnt/ -catenin and NF- B pathways via regulating CXCR4. The present study demonstrated that UCA1 
inhibition exerted an antigrowth and antimigration role in MHCC97 cells through regulating miR-301a and 
CXCR4 expression.},
DOI = {10.3727/096504018X15201143705855}
}