Abstract

AbstractProstate adenocarcinoma PC‐3 and bladder carcinoma J82 cell lines were used to investigate the role of adenosine in the modulation of cell growth. Our results show that adenosine inhibited cell proliferation in both cell lines and markedly induced apoptosis only in J82 cells. PC‐3 and J82 cells showed typical sigmoid growth curves. Only the J82 growth curve was modified by the addition of adenosine deaminase, indicating that this cell line is sensitive to the presence of endogenous extracellular adenosine. Exogenous extracellular adenosine induced a dose‐dependent decrease of cell growth in both cell lines. 2′‐Deoxyadenosine and dipyridamole were used to investigate whether the growth inhibitory effect of adenosine was related to cellular uptake or to receptor‐mediated action. Our results show that 2′‐deoxyadenosine was a less effective inhibitor for J82 than PC‐3 cells. Dipyridamole reduced the inhibitory effect of adenosine in both cell lines. The determination of viability associated with Hoechst staining showed that adenosine clearly induced apoptosis in J82 cell lines but was less effective in PC‐3 cell lines. In conclusion, we have shown that the growth of prostate adenocarcinoma PC‐3 and bladder carcinoma J82 cell lines is inhibited by adenosine and that adenosine is capable of inducing apoptosis, although to a different extent in both cell lines. Drug Dev. Res. 58:390–395, 2003. © 2003 Wiley‐Liss, Inc.

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