Yoshinouchi M, Hongo A, Takamoto N, Ono Y, Nagao S, Miyagi Y, Kudo T, Kodama J
Department of Obstetrics, Okayama University Medical School, Okayama 700-8558, Japan.
Int J Oncol. 2000 Mar;16(3):537-41. doi: 10.3892/ijo.16.3.537.
To determine whether alterations of the CDKN2/p16 might be involved in HPV-positive cervical cancers, we examined for alterations of this gene and function of the protein p16 to interact with CDK4 in 5 cervical cancer cell lines. No alteration of this gene was detected. Proteins for p16 and CDK4 were normally expressed and function of p16 to interact with CDK4 was not abrogated in these cell lines. These cell lines were human papillomavirus (HPV)-positive and carried wild-type p53. These findings suggest that phosphorylation of pRb by CDK4 is not critical in the carcinogenesis or in the establishment of HPV-positive cervical cancer cell lines, since HPV E6 or E7 viral-transforming proteins inactivate p53 and pRb tumor suppressor protein function, resulting in deregulated progression of the cell cycle.
为了确定CDKN2/p16的改变是否可能与HPV阳性宫颈癌有关,我们检测了5种宫颈癌细胞系中该基因的改变以及p16蛋白与CDK4相互作用的功能。未检测到该基因的改变。p16和CDK4蛋白正常表达,且在这些细胞系中p16与CDK4相互作用的功能未被消除。这些细胞系为人乳头瘤病毒(HPV)阳性,并携带野生型p53。这些发现表明,CDK4对pRb的磷酸化在HPV阳性宫颈癌细胞系的致癌过程或建立过程中并不关键,因为HPV E6或E7病毒转化蛋白会使p53和pRb肿瘤抑制蛋白功能失活,导致细胞周期进程失控。