Aim:To explore the effect of androgen receptor (AR) on the expression of the cell cycle-related genes,such asCDKN1A and BTGI,in prostate cancer cell line LNCaE Methods:After AR antagonist flutamide treatment andconfirmation of its effect by phase contrast microscope and flow cytometry,the differential expression of the cellcycle-related genes was analyzed by a cDNA microarray.The flutamide treated cells were set as the experimentalgroup and the LNCaP cells as the control.We labeled cDNA probes of the experimental group and control group withCy5 and Cy3 dyes,respectively,through reverse transcription.Then we hybridized the cDNA probes with cDNAmicroarrays,which contained 8 126 unique human cDNA sequences and the chip was scanned to get the fluorescentvalues of Cy5 and Cy3 on each spot.After primary analysis,reverse transcription polymerase chain reaction (RT-PCR) tests were carried out to confirm the results of the chips.Results:After AR antagonist flutamide treatment,three hundred and twenty-six genes (3.93 %) expressed differentially,97 down-regulated and 219 up-regulated.Among them,eight up-regulated genes might be cell cycle-related,namely CDCIO,NRAS,BTG1,Weel,CLK3,DKFZP564A122,CDKN1A and BTG2.The CDKN1A and BTG1 gene mRNA expression was confirmed to be higherin the experimental group by RT-PCR,while p53 mRNA expression had no significant changes.Conclusion:Flutamidetreatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells.The protein expressions ofCDKNIA and BTG1 play an important role in inhibiting the proliferation of cancer cells.CDKN1A has a great impacton the cell cycle of prostate cancer cells and may play a role in the cancer cells in a p53-independent pathway.Theprostate cancer cells might affect the cell cycle-related genes by activating AR and thus break the cell cycle control.(Asian J Androl 2005 Dec;7:375-380) Aim: To explore the effect of androgen receptor (AR) on the expression of the cell cycle-related genes, such as CDKN1A and BTGI, in prostate cancer cell line LNCaE Methods: After AR antagonist flutamide treatment and confirmation of its effect by phase contrast microscope and flow cytometry, the differential expression of the cellcycle-related genes was was analyzed by a cDNA microarray. fltamide treated cells were set as the experimental group and the LNCaP cells as the control. Weighed cDNA probes of the experimental group and control group with Cy5 and Cy3 dyes, respectively, through reverse transcription. Chen we hybridized the cDNA probes with cDNA microarrays, which contained 8 126 unique human cDNA sequences and the chip was scanned to get the fluorescent values ​​of Cy5 and Cy3 on each spot. After primary analysis, reverse transcription polymerase chain reaction (RT-PCR) tests were carried out to confirm the results of the chips. Results: After AR antagonist flutamide treatment, three hundred and Eighty-six genes (3.93%) were expressed differentially, 97 down-regulated and 219 up-regulated. Among them, eight up-regulated genes might be cell cycle-related, namely CDCIO, NRAS, BTG1, Weel, CLK3, DKFZP564A122, CDKN1A and BTG2.The CDKN1A and BTG1 gene mRNA expression was confirmed to be higher in the experimental group by RT-PCR, while p53 mRNA expression had no significant changes. Conflux: Flutamidetreatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells.The protein expressions of CDKNIA and BTG1 play an important role in inhibiting the proliferation of cancer cells. CDKN1A has a great impact on the cell cycle of prostate cancer cells and may play a role in the cancer cells in a p53-independent pathway. Theprostate cancer cells might affect the cell cycle-related genes by activating AR and thus break the cell cycle control. (Asian J Androl 2005 Dec; 7: 375-380)