TFAP4 promotes the growth of prostate cancer cells by upregulating FOXK1

Transcription factor activating enhancer binding protein 4 (TFAP4) has been indicated to be correlated with the progression of various human malignancies. However, the effect and regulatory mechanism of TFAP4 in prostate cancer (PC) remain unclear. The protein and mRNA expression were detected by western blotting and RT-qPCR. TFAP4 was overexpressed or knocked down in PC cells. The viability, invasion and migration of PC cells were analyzed by CCK-8, Transwell and wound healing assays. The colony formation was also determined. TFAP4 expression was upregulated in PC patients and cells; high TFAP4 expression predicted poor prognosis, and was associated with a range of clinicopathological features, including metastasis, clinical stage and Gleason score. Moreover, overexpression of TFAP4 promoted cell viability, migration, and invasion in vitro, whereas knockdown of TFAP4 revealed the opposite results. TFAP4 also positively regulated forkhead box K1 (FOXK1) expression. In addition, overexpression of FOXK1 reversed the effects of TFAP4 knockdown on PC cells. These findings clarified the biologic significance of TFAP4 in PC progression and revealed an association between TFAP4 and FOXK1, thus providing a new potential target for clinical therapy of PC.

Automated summary

TFAP4 overexpression in prostate cancer is associated with poor prognosis, promoting cell migration and invasion, and positively regulating FOXK1 expression. Targeting the TFAP4-FOXK1 axis may offer a new approach for clinical therapy in PC.