@Article{096504017X15120379906339,
AUTHOR = {Amanda Ikegami, Luiz Felipe S. Teixeira, Marina S. Braga, Matheus Henrique Dos S. Dias, Eduardo C. Lopes, Maria Helena Bellini},
TITLE = {Knockdown of NF-κB1 by shRNA Inhibits the Growth  of Renal Cell Carcinoma In Vitro and In Vivo},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {5},
PAGES = {743--751},
URL = {http://www.techscience.com/or/v26n5/56687},
ISSN = {1555-3906},
ABSTRACT = {Renal cell carcinoma (RCC) accounts for approximately 2%–3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the 
biggest obstacles to the effective treatment of RCC. The NF-kB transcription factor is one of several molecules 
identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have 
demonstrated the activation of NF-kB in RCC, and many have implicated NF-kB1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-kB1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-kB1 gene led to a 
reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G<sub>2</sub>/M 
arrest in the cells. In addition, immunoblotting analysis revealed a significant increase in cyclin B1 and Bax. 
In vivo experiments showed that Renca-shRNA-NF-kB1 cells have significantly diminished tumori genicity. 
Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-kB1 
tumors. Thus, this study indicates that downregulation of NF-kB1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-kB1 may be a potential therapeutic target for RCC.},
DOI = {10.3727/096504017X15120379906339}
}