IN-VITRO CHARACTERIZATION OF DIHYDROTESTOSTERONE-INDUCED, EPIDERMAL GROWTH FACTOR-INDUCED AND BASIC FIBROBLASTIC GROWTH FACTOR-INDUCED MODIFICATIONS IN THE GROWTH DYNAMICS OF THE HUMAN PROSTATE-CANCER CELL-LINE LNCAP, DU145 AND PC3

Citation
T. Janssen et al., IN-VITRO CHARACTERIZATION OF DIHYDROTESTOSTERONE-INDUCED, EPIDERMAL GROWTH FACTOR-INDUCED AND BASIC FIBROBLASTIC GROWTH FACTOR-INDUCED MODIFICATIONS IN THE GROWTH DYNAMICS OF THE HUMAN PROSTATE-CANCER CELL-LINE LNCAP, DU145 AND PC3, International journal of oncology, 7(5), 1995, pp. 1219-1225
Citations number
40
Categorie Soggetti
Oncology
ISSN journal
10196439
Volume
7
Issue
5
Year of publication
1995
Pages
1219 - 1225
Database
ISI
SICI code
1019-6439(1995)7:5<1219:ICODEG>2.0.ZU;2-4
Abstract
The influence of dihydrotestosterone (DHT), the epithelial growth fact or (EGF) and the basic fibroblast growth factor (bFGF) was investigate d on LNCaP, DU145 and PC3 cell growth, which represents the ratio betw een cell gain (cell proliferation) and cell loss (cell death). In the present study, cell growth was assessed by means of the computer-assis ted microscope analysis of Feulgen-stained nuclei combined with the ma thematical Delaunay triangulation and Voronoi paving techniques, which enabled the cell colony patterns, i.e. their density and level of org anisation, to be determined. The results from a previous study (Jansse n et al, Prostate, in press) combined with those of the present one sh ow that DHT was found to activate proliferation of the LNCaP model, as evidenced by increase in size of colonies, increase in number of cell s within colonies, increase in cell colony density and, accordingly, d ecrease in mean segment length value (which is the distance between ad jacent cell nuclei). Using the same criteria, DHT was found inhibitory on growth of DU145 cell line, and devoid of significant effect on PC3 cell line. Basic FGF was found to be a powerful stimulator of growth of PC3 cell Line and to induce a weaker stimulation of DU145 cell line . On LNCaP cell line, it increased the size of colonies without increa se of the number of cells per colony. This feature can be explained by a decrease in cell colony density. With respect to the same colonies, the proliferation index (percentage of cells in the S+G2 phases of th e cell cycle) was found similar to that of the controls. This suggests that the increase in the size of the colonies is due to a difference of spreading of the cells on their supports. EGF had no significant ef fect on LNCaP and PC3 models, and was decreasing cell density of DU145 colonies.