Effects of exogenous lactoferrin on phenotypic profile and invasiveness of human prostate cancer cells (DU145 and LNCaP) in vitro

• Published in: Experimental oncology Vol. 40; no. 3; p. 184
• Main Authors: Zadvornyi, T V, Lukianova, N Yu, Borikun, T V, Chekhun, V F
• Format: Journal Article
• Language: English
• Published: Ukraine 01.10.2018
• Subjects: Cadherins - genetics; Cell Line, Tumor; Estrogen Receptor alpha - genetics; Gene Expression Regulation, Neoplastic - drug effects; Humans; Ki-67 Antigen - genetics; Lactoferrin - pharmacology; Male; MicroRNAs - genetics; Neoplasm Invasiveness - genetics; Neoplasm Invasiveness - pathology; Prostatic Neoplasms - drug therapy; Prostatic Neoplasms - genetics; Prostatic Neoplasms - pathology; Receptor, ErbB-2 - genetics; Receptors, Androgen - genetics
• ISSN: 1812-9269
• DOI: 10.31768/2312-8852.2018.40(3):184-189

To investigate the biological effects of exogenous lactoferrin (LF) on phenotypic profile and invasiveness of human prostate cancer (PC) cells in vitro. Human PC cell lines (LNCaP, DU-145) were cultured with an exogenous LF at a dose corresponding to IC30. The expression levels of steroid hormone receptors (androgen receptor, estrogen receptor, progesterone receptor), Her2/neu, Ki-67, E- and N-cadherin, were monitored by immunohistochemical analysis. The levels of miRNAs were assessed using q-PCR. The invasive activity of the cells was examined in a standard invasion test. Exogenous LF reduced expression of steroid hormone receptors (ERα and PR) and Ki-67 in both PC cell lines. The expression of E-cadherin increased significantly in LF-treated DU-145 cells. Also, we established the decrease in invasive activity upon LF treatment by 40% and 30% in DU-145 and LNCaP cells, respectively. In DU-145 cells, incubation with exogenous LF resulted in an increase in the expression of oncosuppressive (miR-133a and miR-200b) miRNAs. Exogenous LF causes the changes in phenotypic characteristics of PC cells and levels of oncogenic and oncosuppressive miRNAs involved in the regulation of key cellular processes.