Transient exposure to cytarabine increases peptide growth factor receptor expression and tumorigenicity of melanoma cells
Caraglia, M.; Leardi, A.I.; Improta, S.; Perin, V.; Ricciardi, B.; Arra, C.; Ferraro, P.; Fabbrocini, A.; Pinto, A.; Bianco, A.R.; Tagliaferri, P.
Anticancer Research 17(4a): 2369-2375
1997
ISSN/ISBN: 0250-7005 PMID: 9252649 Document Number: 480909
We have demonstrated that anticancer drugs at cytostatic concentrations enhance the expression and function of epidermal growth factor (EGF-R) and transferrin (TRF-R) receptors on human tumor cells. We hypothesized that these effects could represent a protective response of tumor cells to sublethal antiproliferative stimuli which could lead to enhanced growth potential. 72 hours exposure of human melanoma GLL-19 cells to 1,000 nM ara-C induced growth inhibition and increased the number of EGF-R, TRF-R and nerve growth factor receptor (NGF-R) on cell surface. Enhanced expression of beta-3 integrins CD49a, CD49c and CD49e, a-v integrin CD51, beta-3 integrin CD61, CD58/LFA3 and collagen IV and laminin was also detected in ara-C-treated GLL-19 cells. These changes at the tumor cell surface were paralleled by increased in vitro adhesion, invasive potential and clonogenic growth in soft agar and in vivo tumor formation. A more aggressive tumor cell phenotype is induced in human melanoma cells after transient exposure to cytostatic concentrations of ara-C.