Premium
Gene amplification of atypical PKC‐binding PARD3 in radiation‐transformed neoplastic retinal pigment epithelial cell lines
Author(s) -
Zitzelsberger Horst,
Hieber Ludwig,
Richter Hedwig,
Unger Kristian,
Briscoe Cecilia V.,
Peddie Clare,
Riches Andrew
Publication year - 2004
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.20024
Subject(s) - biology , neoplastic transformation , carcinogenesis , microbiology and biotechnology , cell culture , cancer research , positional cloning , gene , genetics , mutant
Neoplastic transformation induced by ionizing radiation was studied using a human retinal pigment epithelial cell line immortalized by telomerase. Radiation‐transformed cell clones were tumorigenic in athymic mice and were analyzed by G‐banding and comparative genomic hybridization (CGH). Radiation‐transformed cloned cell lines and cell lines derived from tumors produced in athymic nude mice following transplantation exhibited a recurrent karyotype:45,XX,der(10),‐13. CGH showed an amplification of 10p11.2 and a deletion of the remaining 10p. Positional cloning of the amplified region by FISH analysis and subsequent sequence analysis of BAC clones showing amplified FISH signals identified the candidate gene PARD3 . This gene also was found to be transcriptionally expressed at an increased level. The findings indicate that PARD3 may play an important role in radiation‐induced carcinogenesis of RPE cells. This is the first evidence for PARD3 amplification in human cancer cells. © 2004 Wiley‐Liss, Inc.