作者: Peter Ly , Ugur Eskiocak , Sang B. Kim , Andres I. Roig , Suzie K. Hight
DOI: 10.1593/NEO.101580
关键词:
摘要: Chromosomal instability leading to aneuploidy occurs in most sporadic colorectal cancers (CRCs) and is believed be an early driving force disease progression. Despite this observation, the cellular advantages conferred by these cytogenetic alterations are poorly understood. Here, we provide evidence that serum-free passage of originally diploid, immortalized human colonic epithelial cells (HCECs) gave rise acquisition trisomy 7 (+7), detected more than 40% adenomas. These remain diploid under long-term growth 2% serum conditions. Analysis GTG banding fluorescent situ hybridization no rare preexisting +7 cell original population, suggesting a conversion aneuploid state. The also precedes loss or truncation adenomatosis polyposis coli gene as both express full-length, functional protein. Coculturing fluorescent-labeled demonstrate HCECs have advantage over Defects migration aberrant regulation epidermal factor receptor, located on chromosome 7p, HCECs. Interestingly, knockdown TP53 expression K-RasV12 resulted emergence 20, another nonrandom observed ∼85% CRC. In summary, describe isogenic represent changes occurring frequently characterization 20 may serve unique cell-based models examine effects chromosomal CRC