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SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer

Lianjie Li1, Chuan Shen1, Eijiro Nakamura1

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Cancer Cell
|December 17, 2013
PubMed

Insights

Clear cell renal cell carcinoma (ccRCC) involves chromosome 5q gain, leading to SQSTM1 oncogene overexpression. This drives cancer progression by promoting redox stress resistance and tumor growth.

Area of Science:

  • Oncology
  • Cancer Genetics

Background:

  • Clear cell renal cell carcinoma (ccRCC) is the most common kidney cancer subtype.
  • ccRCC is characterized by specific chromosomal alterations, including 3p loss (VHL gene), 14q loss (HIF1A), and 5q gain.

Purpose of the Study:

  • To identify the specific target gene(s) on chromosome 5q responsible for ccRCC development.
  • To investigate the role of 5q amplification in ccRCC pathogenesis.

Main Methods:

  • Analysis of ccRCC cell lines and tumor samples.
  • Investigating the effect of SQSTM1 (sequestosome 1) gene expression.
  • Assessing cellular responses to redox stress and tumor formation in vitro and in vivo.

Main Results:

  • 5q amplification in ccRCC correlates with increased SQSTM1 oncogene expression.
  • Elevated SQSTM1 enhances resistance to redox stress and promotes anchorage-independent growth (soft agar).
  • Reduced SQSTM1 impairs cellular fitness, diminishes redox stress resistance, and decreases tumor formation.

Conclusions:

  • SQSTM1 is a key oncogene on chromosome 5q driving ccRCC.
  • The amplification of 5q in ccRCC is, in part, selected for due to the oncogenic functions of SQSTM1.

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