TY  - EJOU
AU  - Ikegami, Amanda 
AU  - Teixeira, Luiz Felipe S. 
AU  - Braga, Marina S. 
AU  - Dias, Matheus Henrique Dos S. 
AU  - Lopes, Eduardo C. 
AU  - Bellini, Maria Helena 

TI  - Knockdown of NF-κB1 by shRNA Inhibits the Growth  of Renal Cell Carcinoma In Vitro and In Vivo
T2  - Oncology Research

PY  - 2018
VL  - 26
IS  - 5
SN  - 1555-3906

AB  - 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.
KW  - Renal cell carcinoma (RCC); Proliferation; Short hairpin RNA (shRNA); Nuclear factor κ-light-chain-enhancer of activated B cells 1 (NF-κB1)

DO  - 10.3727/096504017X15120379906339