[Growth inhibition effect of 5-aza-CdR on endometrial carcinoma xenografted in nude mice by p16 gene demethylation].
OBJECTIVE
To study the antitumor effect and mechanism of 5-aza-CdR on endometrial carcinoma xenografted in nude mice.


METHODS
The effects of 5-aza-CdR on tumor growth inhibition were observed on human endometrial carcinoma xenografted in nude mice. The methylation status of the 5' CpG island of the p16 gene was evaluated using methylation-sensitive restriction enzymes and polymerase chain reaction. p16 mRNA expression was determined by reverse transcription-polymerase chain reaction.


RESULTS
The inhibition rates of the tumor were 79.10% in 5-aza-CdR group (P < 0.01), 90.32% in 5-aza-CdR + DDP group (P < 0.01), and 10.13% in DDP group (P > 0.05), respectively, in comparison with control group. The methylation level of p16 gene was gradually decreased and the p16 mRNA expression restored after exposure to 5-aza-CdR.


CONCLUSIONS
Our data show that 5-aza-CdR may inhibit tumor growth by reactivating growth-regulatory gene silenced by de novo methylation.
Chao
H
H
Department of Gynecology, Chinese Academy of Medical Sciences, Beiking Union Medical College, Beijing 100021, China.
Sun
J
J
Lu
S
S
D000818:Animals; D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use*; D001374:Azacitidine / Q000494:pharmacology / Q000627:therapeutic use*; D019175:DNA Methylation; D016889:Endometrial Neoplasms / Q000188:drug therapy*; D005260:Female; D019942:Genes, p16 / Q000502:physiology*; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D012333:RNA, Messenger; D014183:Transplantation, Heterologous
D000964:Antimetabolites, Antineoplastic; D012333:RNA, Messenger; D001374:Azacitidine