SCD5, SPTBN1, FABP5, SQLE, PTPLA (HACD1), and CDC25B transcription levels were of high prognostic value, which might assist us to understand the underlying carcinogenesis or advancement of UVM better.
Collectively, our study demonstrate that KCTD12 binds to CDC25B and activates CDK1 and Aurora A to facilitate the G2/M transition and promote tumorigenesis and that Aurora A phosphorylates KCTD12 at serine 243 to trigger a positive feedback loop, thereby potentiating the effects of KCTD12.
Both CDC25B and PED/PEA-15 play a certain role in the carcinogenesis of esophageal cancer, and PED/PEA-15 has a greater influence on postoperative survival time.
We postulate that the induction of Cdc25B expression in lung cancer cells by the ultimate carcinogen anti-BPDE accelerates the further development of lung carcinogenesis.