Genetic determinants of FOXM1 overexpression in epithelial ovarian cancer and functional contribution to cell cycle progression.
作者： Carter J. Barger , Wa Zhang , Joanna Hillman , Aimee B. Stablewski , Michael J. Higgins
关键词: FOXM1 、 Cell cycle 、 Cell growth 、 Cancer research 、 Medicine 、 Cell 、 Gene expression profiling 、 Immunology 、 Telomerase reverse transcriptase 、 Retinoblastoma protein 、 Ovarian cancer
摘要: The FOXM1 transcription factor network is frequently activated in high-grade serous ovarian cancer (HGSOC), the most common and lethal subtype of epithelial (EOC). We used primary human EOC tissues, HGSOC cell lines, mouse surface (OSE) cells, a murine transgenic model to investigate genetic determinants overexpression EOC, begin define its functional contribution disease pathology. Cancer Genome Atlas (TCGA) data indicated that locus amplified ~12% HGSOC, greater than any other tumor type examined, amplification correlates with increased expression poor survival. In an independent set correlated advanced stage grade. Of three known isoforms, FOXM1c showed highest EOC. OSE combined knockout Rb1 Trp53 synergistically induced FOXM1. Consistently, cells immortalized SV40 Large T antigen (IOSE-SV) had significantly higher hTERT (IOSE-T). was overexpressed tumors driven by Rb1/Trp53 disruption. induction IOSE-SV partially dependent on E2F1, E2F1 tissues. Finally, functionally contributed cycle progression relevant target gene models. summary, amplification, p53 Rb disruption, activation drive promotes
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