Knockdown of NF-kB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo


Publication type
Article
Appears in Collections:
Metrics
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-kappa B 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-kappa B in RCC, and many have implicated NF-kappa B1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-kappa B1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-kappa B1 gene led to a reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G(2)/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-kappa B1 cells have significantly diminished tumori genicity. Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-kappa B1 tumors. Thus, this study indicates that downregulation of NF-kappa B1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-kappa B1 may be a potential therapeutic target for RCC.
Reference
Ikegami A, Teixeira LFS., Braga MS., Dias MH, Lopes EC, Bellini MH. Knockdown of NF-kB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo. Oncol. Res.. 2018;26(5): 743-51. doi:10.3727/096504017X15120379906339.
Link to cite this reference
https://repositorio.butantan.gov.br/handle/butantan/2490
Journal title
Issue Date
2018


Files in This Item:

10.3727.096504017X15120379906339.pdf
Size: 4.48 MB
Format: Adobe PDF
View/Open
Show full item record

The access to the publications deposited in this repository respects the licenses from journals and publishers.