CDKN2 in HPV-positive and HPV-negative cervical-carcinoma cell lines

✍ Scribed by Michael J. Kelley; Gregory A. Otterson; Frederic J. Kaye; Nicholas C. Popescu; Bruce E. Johnson; Joseph A. Dipaolo

• Book ID: 102866227
• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: French
• Weight: 947 KB
• Volume: 63
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910630214

✦ Synopsis

Human cervical cancers frequently contain retinoblastoma protein (Rb) that is inactivated by binding with human papilloma virus (HPV) E7 protein or through mutation. The CDKNZ gene encodes p 16"" which inhibits cdk4-cyclin D phosphorylation of Rb, preventing the GI-S transition. To determine whether abnormalities of CDKNZ occur in cervical-cancer cells, I I cervical cell lines, including 8 HPV-positive cell lines, 2 HPV-negative cell lines containing mutant Rb. and one tumorigenic cell line derived from normal cervical cells following transfection with HPV-I6 and v-H-ras (CX 16-2HR). were analyzed. No cell line had a homozygous deletion of exon l or 2 of CDKNZ. and only one cell line, CX I6-2HR. had an altered DNA sequence, which represents a common polymorphism at codon 148. To exclude the possibility of other subtle inactivating mutations, imrnunoblot analysis of rotein lysates was performed using a polyclonal anti-p I 6INKBrabbit anti-serum. Abundant levels of normal-sized p16INK4 were observed in all cell samples. Thus, no alterations of CDKNZ were detected in these cervical cell lines. These results confirm that mutational inactivation of p I 6INK4 is a rare event in tumor samples with compromised Rb activity.