tailieunhanh - Báo cáo y học: " Transcriptional regulation of metastatic [Id]entity by KLF17"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Transcriptional regulation of metastatic [Id]entity by KLF17. | X Genome Biology Minireview Transcriptional regulation of metastatic Id entity by KLF17 Marcin P Iwanicki and Joan S Brugge Address Department of Cell Biology Harvard Medical School 240 Longwood Avenue Boston MA 02115 USA. Correspondence Joan S Brugge. Email Joan_Brugge@ Abstract A novel in vivo screening approach has identified KLF17 as a key metastasis suppressor gene that acts through regulation of Id1 transcription factor-dependent induction of the epithelial-to-mesenchymal transition. The development and growth of a malignant tumor relies on molecular changes that affect the function of cellular proto-oncogenes and tumor suppressors 1 . Certain alterations are required constitutively during tumor initiation and progression whereas others are more specifically associated with aspects of tumor metastasis - the spread of malignant cells to secondary tissues. Metastasis suppressors are proteins that specifically repress events associated with metastasis without affecting primary tumor growth 2 . In a recent paper in Nature Cell Biology Huang and colleagues Gumireddy et al. 3 describe experiments that identify a new metastasis suppressor KLF17. The course of metastasis Progression towards metastatic disease involves a distinct sequence of events. Tumor cells attract endothelial cells to promote angiogenesis dissociate from the primary tumor mass and migrate towards endothelial cells intravasate through endothelial cells and the surrounding matrix enter the intra-tumoral vasculature exit the vasculature at the secondary sites infiltrate the new environment and establish growing malignant colonies within a new organ 4 . These events are likely to be driven in large part by changes in transcriptional programs that affect expression of genes required for these processes for example genes that promote angiogenesis cell adhesion and matrix proteolysis . These transcriptional changes are mediated by alterations in the tumor microenvironment 5 as well as by