STAT1 as a potential therapeutic target to treat bladder cancer.

Background: Previous studies have reported that STAT1 (Signal Transducer and Activator of Transcription 1) is associated with multiple tumor progression. This study aimed to investigate the role and related mechanisms of STAT1 in bladder cancer.
Methods: STAT1 expression in bladder cancer tissues and human bladder cancer cell lines was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The bladder cancer cell line T24 was transfected with overexpressing lentivirus targeting STAT1. Cell proliferation, invasion, and apoptosis were measured by Cell Counting Kit-8, Transwell assays, and flow cytometric analysis. Furthermore, RNA-Seq was performed to identify the downstream signaling pathways. Finally, the signaling pathway-related molecules were determined by RT-qPCR and western blot assays.
Results: The overexpression of STAT1 inhibited bladder cancer cell proliferation and invasion while enhancing apoptosis. Moreover, the overexpression of STAT1 in bladder cancer cells delayed tumor tumorigenesis in vitro. Mechanistically, RNA-Seq analysis revealed that the JAK-STAT signaling pathway was up-regulated, especially SOCS1 (suppressor of cytokine signaling 1) and SOCS3 (suppressor of cytokine signaling 3) in STAT1-sufficient cells.
Conclusions: These results indicate the potential of STAT1 as a therapeutic target in bladder cancer.
Competing Interests: None.
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