Abstract
Zinc finger protein 403 (ZFP403), located on human chromosome 17q12‑21, is closely associated with the development of cancer. However, to date, there are a limited number of studies on the biological functions of this gene, particularly in prostate cancer (PCa). The results of the present study demonstrated that compared with normal tissues, the expression of ZFP403 was markedly lower in PCa tissues, as shown by the evaluation of the Gene Expression Profiling Interactive Analysis 2 database. The decreased expression of ZFP403 in PCa clinical tissues and cell lines was confirmed by immunohistochemistry, reverse transcription‑quantitative PCR and western blot analysis. Using short harpin (sh)RNA inhibition, stably‑silenced ZFP403 cell lines were then constructed by lentiviral transfection (LV‑PC3‑shRNA‑1 and 2; LV‑DU145‑shRNA‑1 and 2). The results revealed that the knockdown of ZFP403 in PCa cells promoted cellular proliferation, colony formation, migration and invasiveness in vitro. Moreover, the levels of tumor growth‑ and motility‑related proteins were significantly altered after ZFP403‑knockdown. A xenograft tumor model using nude mice was established to elucidate the role of ZFP403 in tumorigenesis in vivo. Tumor growth was significantly increased in mice injected with ZFP403‑knockdown cells compared with the control mice. Overall, the findings of the present study demonstrate that ZFP403 functions as a tumor suppressor gene in PCa by affecting the proliferation, migration and invasiveness of PCa cells, suggesting its potential use as a clinical diagnostic marker.