Background: Bladder cancer is a complicated disease with high rate of morbidity and mortality, in which proliferation and migration are both well acknowledged as aggressive phenotypes of bladder cancer cells. A better understanding of the mechanisms of tumor proliferation and migration would provide an insight into cancer progression and provide effective therapeutic strategies.
Methods: The expression of RGS20 was detected using qRT-PCR,western blotting and immunohistochemistry. MTT, Colony formation, anchorage-independent growth assay, and transwell assay were used to evaluate the pro-proliferation and pro-migration potential of RGS20 in vitro. Tumor growth was monitored and analyzed in an animal model. Luciferase activity assay, nuclear extract analysis, and multiple blockade of NF-κB were used to evaluate NF-κB signaling activity.
Results: It revealed that RGS20 was significantly upregulated in bladder cancer and increased RGS20 expression correlated significantly with worse 5-year overall survival. Ectopic overexpression of RGS20 accelerated the proliferation and migration of bladder cancer cells, whereas knockdown of RGS20 inhibited these effects. Mechanistically, RGS20 could activate NF-κB signaling, which played a crucial role in RGS20's effects on proliferation, migration, and tumorigenicity of bladder cancer cells.
Conclusion: Our study highlights that RGS20 acted as an oncogene in bladder cancer and a better understanding of RGS20's functions might provide the potential for clinical intervention in this disease.
Keywords: Bladder cancer; Migration; NF-κB signaling; Proliferation; RGS20.
Copyright © 2019. Published by Elsevier Masson SAS.