GSE201875
MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3
The transcription factor MYB proto-oncogene like 2 (MYBL2) plays a critical role in the regulation of gene expression and tumorigenesis. However, the biological function of MYBL2 in bladder cancer (BLCA) remains to be elucidated. Here, we first revealed that MYBL2 was elevated in BLCA tissues and was significantly correlated with clinicopathological parameters and cancer-specific survival of BLCA patients. Phenotypic assays showed that MYBL2 deficiency suppressed the proliferation and migration of BLCA cells in vitro and in vivo, whereas overexpression of MYBL2 contributed to the opposite phenotype. Mechanistically, MYBL2 could bind to the promoter of its downstream target gene cell division cycle-associated protein 3 (CDCA3) and transactivate it, which in turn promoted the malignant phenotype of BLCA cells. Further investigations revealed that MYBL2 interacted with forkhead box M1 (FOXM1) to co-regulate the transcription of CDCA3. In addition, MYBL2 and CDCA3 may activate the Wnt/ß-catenin signaling by inhibiting the suppressor dickkopf-1 (DKK1), thereby regulating the malignant phenotype of BLCA cells. In conclusion, the current study has identified MYBL2 as an oncogene in BLCA. MYBL2 can accelerate the proliferation and metastasis of BLCA through the transactivation of CDCA3. Overall design: To investigate the downstream target genes (signaling) regulated by MYBL2 in BLCA, RNA-seq was performed in 5637 cells treated by siNC/siMYBL2.