The oncoprotein N‑Myc has a carcinogenic effect in numerous types of cancer, and it can cause castration resistance in prostate cancer (PCa), and leads to the development of small cell neuroendocrine cancer by regulating multiple target genes. Immunohistochemical staining, RT‑qPCR, western blotting, wound healing and CCK‑8 assays were used to detect the expression of N‑Myc and FSCN1 as well as AR and CgA at the human level and cell level. The immunohistochemical results revealed that the protein levels of N‑Myc proto‑oncogene protein (N‑Myc) and fascin (FSCN1) in PCa were significantly higher than that of hyperplastic tissues (P<0.05), and there was a weak correlation between them (P=0.002). In vitro, N‑Myc and FSCN1 were overexpressed in LNCaP and C4‑2 cell lines. The results revealed the promoting effect of N‑Myc and FSCN1 on malignant progression of PCa. In addition, the endogenous FSCN1 was knocked down in the C4‑2 cell line, and the results revealed that the silencing of FSCN1 enhanced the expression of N‑Myc and weakened the expression of the neuroendocrine marker CgA. Therefore, the present findings indicated that N‑Myc may promote the malignant process of PCa by regulating FSCN1 and FSCN1 may have a reverse regulatory effect on N‑Myc.
Keywords: prostate cancer; N-Myc; FSCN1; neuroendocrine transformation.