Expression and function of a novel isoform of Sox5 in malignant B cells

Shanique K E Edwards1, Anand Desai2, Yan Liu2

  • 1Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, United States; Graduate Program in Molecular Biosciences, Rutgers University, Piscataway, NJ 08854, United States.

Leukemia Research
|January 15, 2014
PubMed

Insights

Sox5 is upregulated in B cell lymphomas lacking the TRAF3 tumor suppressor. This novel Sox5 isoform inhibits cell cycle progression, suggesting it regulates malignant B cell proliferation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Tumor suppressor TRAF3 (TNFR-associated factor 3) plays a role in B cell malignancies.
  • Dysregulation of gene expression is a hallmark of cancer development.

Purpose of the Study:

  • To investigate the role of Sox5 in B cell lymphomas.
  • To understand the function of Sox5 in malignant B cells.

Main Methods:

  • Utilized a mouse model with B cell-specific deletion of TRAF3.
  • Analyzed gene and protein expression in normal, premalignant, and malignant B cells.
  • Investigated the functional impact of Sox5 overexpression in human multiple myeloma cells.

Main Results:

  • Sox5 was significantly upregulated in B lymphomas from TRAF3-deficient mice.
  • A novel Sox5 isoform was identified in malignant B cells, localized to the nucleus.
  • Sox5 overexpression inhibited cell cycle progression and increased p27 and beta-catenin levels in human multiple myeloma cells.

Conclusions:

  • Sox5 is a key regulator of malignant B cell proliferation.
  • The novel Sox5 isoform plays a critical role in B cell lymphomagenesis.

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