@Article{096504019X15742472027401,
AUTHOR = {Xiao-hui Sun, Wen-jie Fan, Zong-jian An, Yong Sun},
TITLE = {Inhibition of Long Noncoding RNA CRNDE Increases Chemosensitivity  of Medulloblastoma Cells by Targeting miR-29c-3p},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {1},
PAGES = {95--102},
URL = {http://www.techscience.com/or/v28n1/48550},
ISSN = {1555-3906},
ABSTRACT = {Long noncoding RNA CRNDE (CRNDE) recently emerged as a carcinogenic promoter in various cancers 
including medulloblastoma. However, the functions and molecular mechanisms of CRNDE to the acquired 
drug resistance of medulloblastoma are still unclear. The transcript levels of CRNDE were examined in four 
medulloblastoma cell lines exposed to cisplatin treatment, and IC<sub>50</sub> values were calculated. Effects of CRNDE 
knockdown or miR-29c-3p overexpression on cell viability, colony formation, apoptosis, migration, and invasion were assessed using the CCK-8, colony formation assay, flow cytometry, and Transwell assays, respectively. RNA pulldown and RNA-binding protein immunoprecipitation (RIP) were performed to confirm the 
molecular interactions between CRNDE and miR-29c-3p involved in medulloblastoma cells. The in vivo role 
of CRNDE knockdown or miR-29c-3p overexpression on tumor growth and apoptosis was evaluated in a 
xenograft mouse model of human medulloblastoma. The transcript levels of lncRNA CRNDE were significantly higher in cisplatin-treated tumor cells with higher IC50 values. Depletion of CRNDE inhibited tumor cell 
proliferation and colony formation, induced cell apoptosis, and suppressed migration and invasion in medulloblastoma cells. Moreover, overexpression of miR-29c-3p inhibited tumor cell proliferation and colony formation, migration, and invasion, and enhanced apoptosis and chemosensitivity to cisplatin. In addition, CRNDE 
was found to act as a miR-29c-3p sponge. Furthermore, in vivo experiments showed the CRNDE/miR-29c-3p 
interactions involved in medulloblastoma. Our study demonstrates that CRNDE acts as a critical mediator of 
proliferation, apoptosis, migration, invasion, and resistance to chemotherapeutics via binding to and negatively 
regulating miR-29c-3p in medulloblastoma cells. These results provide novel molecular targets for treatment 
of medulloblastoma.},
DOI = {10.3727/096504019X15742472027401}
}