Expression and function of colony-stimulating factors and their receptors in human prostate carcinoma cell lines

BACKGROUND The predeliction for prostate carcinoma cells to metastasize to bone suggests the hypothesis that bone and/or bone marrow‐derived factors may promote prostate carcinoma cell growth or survival, or serve as chemoattractants for these cells. METHODS We screened three prostate carcinoma cell lines, DU‐145, PC‐3, and LNCaP, for the expression of several hematopoiesis‐associated colony‐stimulating factors (CSFs) and their receptors using RT‐PCR (reverse transcriptase‐polymerase chain reaction) and immunohistochemical methods, and examined their functional effects. RESULTS All of these cell lines express granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and macrophage colony‐stimulating factor (M‐CSF), and the DU‐145 and PC‐3 lines express stem‐cell factor (SCF), as determined by RT‐PCR and ELISA. Each of these cell lines expresses the receptors for SCF, GM‐CSF, M‐CSF, and granulocyte colony‐stimulating factor (G‐CSF). M‐CSF enhanced the soft‐agar clonogenicity of PC‐3 and DU‐145 cells, and GM‐CSF stimulated all three cell lines. SCF stimulated the clonogenic growth of DU‐145 cells. G‐CSF marginally abrogated the induction of cell death in the PC‐3 and LNCaP cell lines under serum‐free conditions. GM‐CSF and M‐CSF stimulated modest chemotaxis of PC‐3, DU‐145, and LNCaP cells (most prominently in PC‐3 cells). CONCLUSIONS These data suggest that 1) CSFs may be part of a network of paracrine and autocrine loops that modulate prostate carcinoma cell activity, and 2) the growth‐stimulatory, survival‐enhancing, and/or chemotactic actions of bone marrow‐derived CSFs on prostate carcinoma cells may explain in part why bone is a preferential site of prostatic carcinoma metastases. Prostate 34:80–91, 1998. © 1998 Wiley‐Liss, Inc.