báo cáo khoa học: "Down-regulation of UHRF1, associated with re-expression of tumor suppressor genes, is a common feature of natural compounds exhibiting anti-cancer properties"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Down-regulation of UHRF1, associated with re-expression of tumor suppressor genes, is a common feature of natural compounds exhibiting anti-cancer properties | Alhosin et al. Journal of Experimental Clinical Cancer Research 2011 30 41 http content 30 1 41 Journal of Experimental Clinical Cancer Research REVIEW Open Access Down-regulation of UHRF1 associated with re-expression of tumor suppressor genes is a common feature of natural compounds exhibiting anti-cancer properties Mahmoud Alhosin Tanveer Sharif Marc Mousli Nelly Etienne-Selloum Guy Fuhrmann Valérie B Schini-Kerth and Christian Bronner Abstract Over-expressed in numerous cancers Ubiquitin-like containing PHD Ring Finger 1 UHRF1 also known as ICBP90 or Np95 is characterized by a SRA domain Set and Ring Associated which is found only in the UHRF family. UHRF1 constitutes a complex with histone deacetylase 1 HDAC1 and DNA methyltransferase 1 DNMT1 via its SRA domain and represses the expression of several tumour suppressor genes TSGs including p16INK4A hMLHl BRCA1 and RB1. Conversely UHRF1 is regulated by other TSGs such as p53 and p73. UHRF1 is hypothetically involved in a macro-molecular protein complex called ECREM for Epigenetic Code Replication Machinery . This complex would be able to duplicate the epigenetic code by acting at the DNA replication fork and by activating the right enzymatic activity at the right moment. There are increasing evidence that UHRF1 is the conductor of this replication process by ensuring the crosstalk between DNA methylation and histone modifications via the SRA and Tandem Tudor Domains respectively. This cross-talk allows cancer cells to maintain the repression of TSGs during cell proliferation. Several studies showed that down-regulation of UHRF1 expression in cancer cells by natural pharmacological active compounds favors enhanced expression or re-expression of TSGs suppresses cell growth and induces apoptosis. This suggests that hindering UHRF1 to exert its role in the duplication of the methylation patterns DNA histones is responsible for inducing apoptosis. In this review we present UHRF1 expression as a target .

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