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.
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.
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.