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The Role of SETD8 in genome intergrity Maintenance and Tumoregenesis: Revelation from a Pair of Identical Twins

The Role of SETD8 in Genome Intergrity Maintenance and Tumor...

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2018年（第四十届）浙江省医学会呼吸系病学术年会

作者： Miao Li Hongwei Liao Chen Zhu Yanping Wu Yinfang Wu Xinwei Geng Zhihua Chen Huahao Shen Songmin Ying Wen Li Department of Respiratory and Critical Care Medicine Second Affiliated Hospital Institute of Respiratory Diseases Zhejiang University School of Medicine Department of Pharmacology Zhejiang University School of Medicine

Objective :Pulmonary sarcomatous neoplasms are a rare group of tumors occur in the lung[1]. We received a pair of monozygotic twins discordant for sarcomatoid neoplasms of the right principal bronchus in their early age. Identical twins were grown in the same environment and the genetic similarity was highly consistent, so we thought the very small number of genetic differences between the sisters may be involved in the occurrence of the disaster. As we all know, most human pathogenic genes are caused by mutations in exons. In order to find out novel genes related to the patient’s tumor, exome sequencing which has unique advantages in identifying the causative genes of rare diseases was *** : Exome sequencing was used in the twins mentioned above. Through comparison analysis among the twins and the general population, 11 genes were first screened out. After further siRNA screening of these genes, we identified H4K20-specific histone methyltransferase SETD8 as the most possible participant in tumor occurrence. Two individual siRNAs of SETD8 were used in U2OS and human bronchial epithelium(HBE) cells, cell proliferation, apoptosis, ageing, cell cycle were analyzed. To determine the effect of single nucleotide variation(SNV, T904C) in patient’s setd8, we overexpressed wildtype and mutant SETD8 respectively in cells, immunoprecipitation and mass spectrometry were followed to analysis the differences in interaction with other proteins, we also amplified wildtype and mutant SETD8 protein in vitro to assess their methyltransferase *** : : The silencing of SETD8 inhibited cell proliferation and increased apoptosis in both two cell lines. Cell cycle arrest and DNA damage also occurred without setd8. DNA fiber assay showed that compared with control, cells transfected with setd8 siRNA exhibited slower replication fork speed. Overexpress exogenous wildtype and mutant SETD8, protein interaction analysis revealed that the mutant SETD8 enhanced histone H4

关键词： Exome Sequencing SETD8 genome intergrity Methyltransferase TumourgenesisREFERENCE

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