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CDKN2 in HPV‐positive and HPV‐negative cervical‐carcinoma cell lines
Author(s) -
Kelley Michael J.,
Otterson Gregory A.,
Kaye Frederic J.,
Popescu Nicholas C.,
Johnson Bruce E.,
Dipaolo Joseph A.
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910630214
Subject(s) - cervical carcinoma , carcinoma , medicine , oncology , cancer research , biology , cervical cancer , cancer
Human cervical cancers frequently contain retinoblastoma protein (Rb) that is inactivated by binding with human papilloma virus (HPV) E7 protein or through mutation. The CDKN2 gene encodes p 16 INK4 which inhibits cdk4‐cyclin D phosphorylation of Rb, preventing the G 1 ‐S transition. To determine whether abnormalities of CDKN2 occur in cervical‐cancer cells, 11 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‐16 and v‐H‐ras (CX16‐2HR), were analyzed. No cell line had a homozygous deletion of exon 1 or 2 of CDKN2 , and only one cell line, CX16‐2HR, had an altered DNA sequence, which represents a common polymorphism at codon 148. To exclude the possibility of other subtle inactivating mutations, immunoblot analysis of protein lysates was performed using a polyclonal anti‐p 16 INK4 rabbit anti‐serum. Abundant levels of normal‐sized pl6 INK4 were observed in all cell samples. Thus, no alterations of CDKN2 were detected in these cervical cell lines. These results confirm that mutational inactivation of p 16 INK4 is a rare event in tumor samples with compromised Rb activity.