Gene-dosage dependent overexpression at the 13q amplicon identifies DIS3 as candidate oncogene in colorectal cancer progression.
作者： Florence L.M. de Groen , Oscar Krijgsman , Marianne Tijssen , Lianne E.M. Vriend , Bauke Ylstra
DOI: 10.1002/GCC.22144
关键词: Colorectal adenoma 、 Cancer research 、 Gene dosage 、 Amplicon 、 Oncogene 、 Biology 、 Candidate gene 、 Molecular biology 、 Chromosome 13 、 Carcinoma 、 Adenoma
摘要: Colorectal cancer (CRC) development is in most cases marked by the accumulation of genomic alterations including gain entire q-arm chromosome 13. This aberration occurs 40%-60% all CRC and associated with progression from adenoma to carcinoma. To date, little known about effect 13q amplicon on expression therein located genes their functional relevance. We therefore aimed identify candidate at that contribute colorectal carcinoma a gene dosage-dependent manner. Integrative analysis whole genome DNA copy number signatures resulted identification 36 which significant overexpression carcinomas compared adenomas was linked gain. Five showing high levels versus were further tested quantitative reverse transcription-PCR two independent sample sets tumors (n = 40 n = 47). DIS3 LRCH1 revealed dependent Silencing affected important tumorigenic characteristics such as viability, migration, invasion. In conclusion, specific 13q. The relevance this corroborated for DIS3, thereby identifying novel oncogene contributing 13q-driven progression.
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