<i>Cordyceps militaris</i> Extract and the Main Component, Cordycepin, Modulate the Functions of Prostate Cancer Cells Partially Through the Adenosine A1 Receptor

Our previous study demonstrated that an extract of Cordyceps militaris (CM) derived from Samia Cynthia ricini inhibits testosterone-induced prostate hypertrophy in animal model. However, the bioactive components CM modulate function cells have not been identified and characterized. To do this, present explored effective component(s) influences viability androgen-responsive LNCaP cancer androgen-independent PC3 cells. Several fractions CM, separated by gel filtration chromatography, decreased proliferation both types either presence or absence testosterone propionate (TP). The reduced TP-induced expression androgen-regulated genes FKBP5, TMPRSS2, KLK3. NMR cordycepin, adenosine, uridine as active fractions. was inhibited but adenosine uridine. Cordycepin, TP-mediated increases FKBP5 TMPRSS2 expression, phosphorylation androgen receptor. Specific A1, A2, A3 receptor antagonists did block inhibitory effects cordycepin on cell proliferation, whereas A1 antagonist CPDPX (8-cyclopentyl-1,3-dipropylxanthine) reversed cordycepin-mediated inhibition expression. Thus, exhibited receptor–independent receptor–dependent effects. These findings suggest independently receptors, its modulatory effect gene is mediated through