Down-regulation of ASY/Nogo transcription associated with progression of adult T-cell leukemia/lymphoma

Int J Cancer. 2006 Oct 1;119(7):1648-53. doi: 10.1002/ijc.22011.

Abstract

Adult T-cell leukemia/lymphoma (ATLL) is an aggressive form of human leukemia/lymphoma. Although this disease is initiated by infection with human T-lymphotropic virus type 1 (HTLV-1), many HTLV-1 carriers survive for a long period without aggressive illness, suggesting that other factors may play roles in the progression of ATLL to an aggressive state. However, the mechanism involved in this progression still remains unclear. Previously, we have reported that ASY/Nogo mRNA was markedly down-regulated in human small-cell lung carcinomas, whereas it was expressed in normal tissues and other lung carcinomas, such as adenocarcinoma and squamous cell carcinoma. To understand whether or not ASY/Nogo gene is involved in the progression of ATLL, we examined the expression of ASY/Nogo mRNA in smoldering, chronic and aggressive ATLL, and found that the expression level of ASY/Nogo mRNA was markedly reduced in clinically aggressive ATLL. HTLV-1 Tax expression was not affected by the down-regulation of ASY/Nogo mRNA. These results indicate that the ASY/Nogo gene may act as a suppressor against ATLL progression, independent of Tax expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Disease Progression
  • Down-Regulation / genetics*
  • Female
  • Gene Expression Regulation, Neoplastic / genetics*
  • Gene Products, tax / genetics
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Leukemia-Lymphoma, Adult T-Cell / genetics*
  • Leukemia-Lymphoma, Adult T-Cell / pathology*
  • Male
  • Membrane Proteins / genetics*
  • Middle Aged
  • Myelin Proteins / genetics*
  • Nogo Proteins
  • RNA, Messenger / genetics
  • Transcription, Genetic / genetics*

Substances

  • Gene Products, tax
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • Myelin Proteins
  • Nogo Proteins
  • RNA, Messenger
  • RTN4 protein, human