Conclusion
Our results uncovered transcription factor YY1 as a positive regulator of NUP93 expression, and NUP93 serves as an oncogenic factor to sustain the malignancy of bladder cancer cells. These findings suggest that targeting the YY1-NUP93 axis could offer novel therapeutic strategies for bladder cancer treatment.
Methods
NUP93 expressions in bladder cancer tissues and normal counterparts were analyzed using a public dataset and clinical samples. NUP93 and Yin Yang 1 (YY1) mRNA expression and protein levels in T24 and RT4 cells were determined by Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The effect of NUP93 knockdown on the proliferation, migration, and invasion capabilities of cells was evaluated. Concurrently, transcriptional regulation of NUP93 by YY1 was confirmed using a dual luciferase assay. The effect of NUP93 knockdown on tumorigenesis was evaluate in a subcutaneous xenograft mouse model.
Objective
This study aims to investigate the functional interplay between transcription factor YY1 and nucleoporin 93 (NUP93) in regulating the malignancy of bladder cancer cells.
Results
Elevated levels of NUP93 in bladder cancer tissues and cell lines were observed. Silencing NUP93 significantly suppressed glycolysis, impeded the growth, migration, invasion and tumor formation of bladder cancer cells. The transcription factor YY1 acted as a positive regulator to upregulate NUP93 expression. YY1 overexpression partially rescued the effects of NUP93 silencing on bladder cancer cells.