On Sept., 26, the research group Prof. Liu Yu and Pro. Chen Chong, in the State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, published an article titled “An Epigenetic Mechanism Underlying Chromosome 17p Deletion-driven Tumorigenesis” online on Cancer Discovery (impact factor 29.5). This article demonstrated a new epigenetic mechanism under which chromosome 17p deletion promotes the tumor development.

Genomic instability is a marked feature of cancer. More than 90% of human tumors contain the copy number variation(CNV) of chromosome. Among them, chromosome 17p deletions happen most frequently, often associated with poor prognosis. In 2016, Liu-Chen group published an article in Nature titled “Deletions Linked to TP53 Loss Drive Cancer Through p53 Independent Mechanisms”, which has proved for the first time that the chromosome 17p large fragment deletion as a whole could drive tumorigenesis in both p53-dependent and –independent way (Liu and Chen et al., Nature 2016). Followed this story, Liu-Chen team further identified a new tumor suppressor gene PHF23 on the chromosome 17p with the combination of RNA interference, gene editing and genetically engineered mouse technologies. Furthermore, multi-omics analyses including Co-IP/MS, ChIP-seq and RNA-seq were applied to investigate the molecular mechanisms under which PHF23 performs tumor suppressive function. They found that PHF23 forms a new epigenetic protein machine with SIN3-HDAC complex, which regulates the downstream gene expressions through correlating histone modifications H3K4me3 and H3K27ac. Finally, their results support that HDAC may be a potential therapeutic target for tumors with chromosome 17p deletions.

West China Hospital of Sichuan University is the first and corresponding institute of this paper; Dr. Chen Mei and Dr. Chen Xuelan of the State Key Laboratory of Biotherapy, are the first co-authors; and Prof. Liu Yu and Prof. Chen Chong of the State Key Laboratory of Biotherapy of WCH are the co-corresponding authors.