Fibronectin influences cellular proliferation and apoptosis similarly in LNCaP and PC-3 prostate cancer cell lines

The mechanisms responsible for the emergence of clinically advanced prostat e cancer (PC) are incompletely understood. Recent studies suggest that alte red tumoral apoptosis with disordered cell proliferation sustains advanced disease and may account for the phenomena of anti-androgen therapeutic resi stance. Previous inquiry has focused primarily on faulty intracellular mech anisms with limited scrutiny of the extracellular matrix including fibronec tin and collagen type 4. We evaluated cell proliferation with Ki-67 immunoa ssay/image analysis and apoptosis by TUNEL staining and Bcl-2 immunoassay/i mage analysis in LNCaP and PC-3 human PC cell lines at baseline and followi ng propagation on fibronectin and collagen type 4-coated coverslip substrat e. Cell cultures showed differing proliferative and apoptosis characteristi cs at baseline, with the LNCaP cell line showing relatively higher prolifer ation and apoptosis rates than the PC-3 cell line. Cell proliferation and a poptosis were statistically significantly decreased in both cell lines foll owing propagation on fibronectin. Bcl-2 expression was significantly increa sed among both cell lines following propagation on fibronectin. In contrast , cell proliferation, apoptosis, and Bcl-2 expression showed insignificant changes in both cell lines following uncoated coverslip and collagen type 4 matrix propagation. Our findings showed that fibronectin influences cell p roliferation, apoptosis. and Bcl-2 expression similarly among LNCaP and PC- 3 PC cell lines. It is likely that the altered rates are independent of the androgen status of the cell line and are mediated through a nonhormonal me chanism. (C) 2000 Elsevier Science Inc. All rights reserved.