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

Abstract

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.