Other
20 Authors
- Marcucci G,
- Yu L,
- Mitsui T,
- Huang K,
- Belyavsky AV,
- Ershler M,
- Yokohama A,
- Liu Z,
- Visser J,
- Liu X,
- Caligiuri MA,
- Liu C,
- Wei M,
- Hackanson B,
- Mao H,
- Trotta R,
- Plass C,
- Yu J,
- Liu S,
- Liu CG
| First Author | Yu J | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 22 | Pages | 5558-67 |
| PubMed ID | 19329776 | Mgi Jnum | J:148897 |
| Mgi Id | MGI:3847064 | Doi | 10.1182/blood-2009-02-205732 |
| Citation | Yu J, et al. (2009) TSC-22 contributes to hematopoietic precursor cell proliferation and repopulation and is epigenetically silenced in large granular lymphocyte leukemia. Blood 113(22):5558-67 |
| abstractText | Aberrant methylation of tumor suppressor genes can lead to their silencing in many cancers. TSC-22 is a gene silenced in several solid tumors, but its function and the mechanism(s) responsible for its silencing are largely unknown. Here we demonstrate that the TSC-22 promoter is methylated in primary mouse T or natural killer (NK) large granular lymphocyte (LGL) leukemia and this is associated with down-regulation or silencing of TSC-22 expression. The TSC-22 deregulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia, which significantly increased survival of the mice bearing this disease. Ectopic expression of TSC-22 in mouse leukemia or lymphoma cell lines resulted in delayed in vivo tumor formation. Targeted disruption of TSC-22 in wild-type mice enhanced proliferation and in vivo repopulation efficiency of hematopoietic precursor cells (HPCs). Collectively, our data suggest that TSC-22 normally contributes to the regulation of HPC function and is a putative tumor suppressor gene that is hypermethylated and silenced in T or NK LGL leukemia. |
